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Erschienen in: Journal of Cardiovascular Translational Research 6/2018

31.08.2018 | Review

Noncoding RNAs in Cardiac Hypertrophy

verfasst von: Yongqin Li, Yajun Liang, Yujiao Zhu, Yuhui Zhang, Yihua Bei

Erschienen in: Journal of Cardiovascular Translational Research | Ausgabe 6/2018

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Abstract

Cardiac hypertrophy is classified as pathological and physiological hypertrophy. Pathological hypertrophy typically precedes the onset of heart failure, one of the largest contributors to disease burden and deaths worldwide. In contrast, physiological hypertrophy is an adaptive response and protects against adverse cardiac remodeling. Noncoding RNAs (ncRNAs) have drawn significant attention over the last couple of decades, and their dysregulation is increasingly being linked to cardiac hypertrophy and cardiovascular diseases. In this review, we will summarize the profiling, function, and molecular mechanism of microRNAs, long noncoding RNAs, and circular RNAs in pathological cardiac hypertrophy. Additionally, we also review microRNAs responsible for physiological hypertrophy. With better understanding of ncRNAs in cardiac hypertrophy, manipulation of the important ncRNAs will offer exciting avenues for the prevention and therapy of heart failure.
Literatur
1.
Zurück zum Zitat Iismaa, S. E., & Graham, R. M. (2003). Dissecting cardiac hypertrophy and signaling pathways: evidence for an interaction between multifunctional g proteins and prostanoids. Circulation Research, 92(10), 1059–1061.PubMed Iismaa, S. E., & Graham, R. M. (2003). Dissecting cardiac hypertrophy and signaling pathways: evidence for an interaction between multifunctional g proteins and prostanoids. Circulation Research, 92(10), 1059–1061.PubMed
2.
Zurück zum Zitat Shimizu, I., & Minamino, T. (2016). Physiological and pathological cardiac hypertrophy. Journal of Molecular and Cellular Cardiology, 97, 245–262.PubMed Shimizu, I., & Minamino, T. (2016). Physiological and pathological cardiac hypertrophy. Journal of Molecular and Cellular Cardiology, 97, 245–262.PubMed
3.
Zurück zum Zitat Frey, N., & Olson, E. N. (2003). Cardiac hypertrophy: the good, the bad, and the ugly. Annual Review of Physiology, 65, 45–79.PubMed Frey, N., & Olson, E. N. (2003). Cardiac hypertrophy: the good, the bad, and the ugly. Annual Review of Physiology, 65, 45–79.PubMed
4.
Zurück zum Zitat Bagga, S., Bracht, J., Hunter, S., Massirer, K., Holtz, J., Eachus, R., et al. (2005). Regulation by let-7 and lin-4 miRNAs results in target mRNA degradation. Cell, 122(4), 553–563.PubMed Bagga, S., Bracht, J., Hunter, S., Massirer, K., Holtz, J., Eachus, R., et al. (2005). Regulation by let-7 and lin-4 miRNAs results in target mRNA degradation. Cell, 122(4), 553–563.PubMed
5.
Zurück zum Zitat Olsen, P. H., & Ambros, V. (1999). The lin-4 regulatory RNA controls developmental timing in Caenorhabditis elegans by blocking LIN-14 protein synthesis after the initiation of translation. Developmental Biology, 216(2), 671–680.PubMed Olsen, P. H., & Ambros, V. (1999). The lin-4 regulatory RNA controls developmental timing in Caenorhabditis elegans by blocking LIN-14 protein synthesis after the initiation of translation. Developmental Biology, 216(2), 671–680.PubMed
6.
Zurück zum Zitat Guo, H., Ingolia, N. T., Weissman, J. S., & Bartel, D. P. (2010). Mammalian microRNAs predominantly act to decrease target mRNA levels. Nature, 466(7308), 835–840.PubMedPubMedCentral Guo, H., Ingolia, N. T., Weissman, J. S., & Bartel, D. P. (2010). Mammalian microRNAs predominantly act to decrease target mRNA levels. Nature, 466(7308), 835–840.PubMedPubMedCentral
7.
Zurück zum Zitat Bronze-da-Rocha, E. (2014, 2014). MicroRNAs expression profiles in cardiovascular diseases. Biomed Res Int, 985408. Bronze-da-Rocha, E. (2014, 2014). MicroRNAs expression profiles in cardiovascular diseases. Biomed Res Int, 985408.
8.
Zurück zum Zitat Chen, L. J., Xu, R., Yu, H. M., Chang, Q., & Zhong, J. C. (2015). The ACE2/Apelin signaling, microRNAs, and hypertension. International Journal of Hypertension, 2015, 896861.PubMedPubMedCentral Chen, L. J., Xu, R., Yu, H. M., Chang, Q., & Zhong, J. C. (2015). The ACE2/Apelin signaling, microRNAs, and hypertension. International Journal of Hypertension, 2015, 896861.PubMedPubMedCentral
9.
Zurück zum Zitat Pang, K. C., Frith, M. C., & Mattick, J. S. (2006). Rapid evolution of noncoding RNAs: lack of conservation does not mean lack of function. Trends in Genetics, 22(1), 1–5.PubMed Pang, K. C., Frith, M. C., & Mattick, J. S. (2006). Rapid evolution of noncoding RNAs: lack of conservation does not mean lack of function. Trends in Genetics, 22(1), 1–5.PubMed
10.
Zurück zum Zitat Devaux, Y., Zangrando, J., Schroen, B., Creemers, E. E., Pedrazzini, T., Chang, C. P., et al. (2015). Long noncoding RNAs in cardiac development and ageing. Nature Reviews. Cardiology, 12(7), 415–425.PubMed Devaux, Y., Zangrando, J., Schroen, B., Creemers, E. E., Pedrazzini, T., Chang, C. P., et al. (2015). Long noncoding RNAs in cardiac development and ageing. Nature Reviews. Cardiology, 12(7), 415–425.PubMed
11.
Zurück zum Zitat Hansen, T. B., Jensen, T. I., Clausen, B. H., Bramsen, J. B., Finsen, B., Damgaard, C. K., et al. (2013). Natural RNA circles function as efficient microRNA sponges. Nature, 495(7441), 384–388.PubMed Hansen, T. B., Jensen, T. I., Clausen, B. H., Bramsen, J. B., Finsen, B., Damgaard, C. K., et al. (2013). Natural RNA circles function as efficient microRNA sponges. Nature, 495(7441), 384–388.PubMed
12.
13.
Zurück zum Zitat Jeck, W. R., Sorrentino, J. A., Wang, K., Slevin, M. K., Burd, C. E., Liu, J., et al. (2013). Circular RNAs are abundant, conserved, and associated with ALU repeats. RNA, 19(2), 141–157.PubMedPubMedCentral Jeck, W. R., Sorrentino, J. A., Wang, K., Slevin, M. K., Burd, C. E., Liu, J., et al. (2013). Circular RNAs are abundant, conserved, and associated with ALU repeats. RNA, 19(2), 141–157.PubMedPubMedCentral
14.
Zurück zum Zitat Zhang, X. O., Wang, H. B., Zhang, Y., Lu, X., Chen, L. L., & Yang, L. (2014). Complementary sequence-mediated exon circularization. Cell, 159(1), 134–147.PubMed Zhang, X. O., Wang, H. B., Zhang, Y., Lu, X., Chen, L. L., & Yang, L. (2014). Complementary sequence-mediated exon circularization. Cell, 159(1), 134–147.PubMed
15.
Zurück zum Zitat Ashwal-Fluss, R., Meyer, M., Pamudurti, N. R., Ivanov, A., Bartok, O., Hanan, M., et al. (2014). circRNA biogenesis competes with pre-mRNA splicing. Molecular Cell, 56(1), 55–66.PubMed Ashwal-Fluss, R., Meyer, M., Pamudurti, N. R., Ivanov, A., Bartok, O., Hanan, M., et al. (2014). circRNA biogenesis competes with pre-mRNA splicing. Molecular Cell, 56(1), 55–66.PubMed
16.
Zurück zum Zitat Zhang, Y., Zhang, X. O., Chen, T., Xiang, J. F., Yin, Q. F., Xing, Y. H., et al. (2013). Circular intronic long noncoding RNAs. Molecular Cell, 51(6), 792–806.PubMed Zhang, Y., Zhang, X. O., Chen, T., Xiang, J. F., Yin, Q. F., Xing, Y. H., et al. (2013). Circular intronic long noncoding RNAs. Molecular Cell, 51(6), 792–806.PubMed
17.
Zurück zum Zitat Memczak, S., Jens, M., Elefsinioti, A., Torti, F., Krueger, J., Rybak, A., et al. (2013). Circular RNAs are a large class of animal RNAs with regulatory potency. Nature, 495(7441), 333–338. Memczak, S., Jens, M., Elefsinioti, A., Torti, F., Krueger, J., Rybak, A., et al. (2013). Circular RNAs are a large class of animal RNAs with regulatory potency. Nature, 495(7441), 333–338.
18.
Zurück zum Zitat Kapusta, A., & Feschotte, C. (2014). Volatile evolution of long noncoding RNA repertoires: mechanisms and biological implications. Trends in Genetics, 30(10), 439–452.PubMed Kapusta, A., & Feschotte, C. (2014). Volatile evolution of long noncoding RNA repertoires: mechanisms and biological implications. Trends in Genetics, 30(10), 439–452.PubMed
19.
Zurück zum Zitat Ounzain, S., Micheletti, R., Beckmann, T., Schroen, B., Alexanian, M., Pezzuto, I., et al. (2015). Genome-wide profiling of the cardiac transcriptome after myocardial infarction identifies novel heart-specific long non-coding RNAs. European Heart Journal, 36(6), 353–368a.PubMed Ounzain, S., Micheletti, R., Beckmann, T., Schroen, B., Alexanian, M., Pezzuto, I., et al. (2015). Genome-wide profiling of the cardiac transcriptome after myocardial infarction identifies novel heart-specific long non-coding RNAs. European Heart Journal, 36(6), 353–368a.PubMed
20.
Zurück zum Zitat Zhao, Y., Li, H., Fang, S., Kang, Y., Wu, W., Hao, Y., et al. (2016). NONCODE 2016: an informative and valuable data source of long non-coding RNAs. Nucleic Acids Research, 44(D1), D203–D208.PubMed Zhao, Y., Li, H., Fang, S., Kang, Y., Wu, W., Hao, Y., et al. (2016). NONCODE 2016: an informative and valuable data source of long non-coding RNAs. Nucleic Acids Research, 44(D1), D203–D208.PubMed
21.
Zurück zum Zitat Sun, L., Zhang, Y., Zhang, Y., Gu, Y., Xuan, L., Liu, S., et al. (2014). Expression profile of long non-coding RNAs in a mouse model of cardiac hypertrophy. International Journal of Cardiology, 177(1), 73–75.PubMed Sun, L., Zhang, Y., Zhang, Y., Gu, Y., Xuan, L., Liu, S., et al. (2014). Expression profile of long non-coding RNAs in a mouse model of cardiac hypertrophy. International Journal of Cardiology, 177(1), 73–75.PubMed
22.
Zurück zum Zitat Li, X., Zhang, L., & Liang, J. (2016). Unraveling the expression profiles of long noncoding RNAs in rat cardiac hypertrophy and functions of lncRNA BC088254 in cardiac hypertrophy induced by transverse aortic constriction. Cardiology, 134(2), 84–98.PubMed Li, X., Zhang, L., & Liang, J. (2016). Unraveling the expression profiles of long noncoding RNAs in rat cardiac hypertrophy and functions of lncRNA BC088254 in cardiac hypertrophy induced by transverse aortic constriction. Cardiology, 134(2), 84–98.PubMed
23.
Zurück zum Zitat Yang, K. C., Yamada, K. A., Patel, A. Y., Topkara, V. K., George, I., Cheema, F. H., et al. (2014). Deep RNA sequencing reveals dynamic regulation of myocardial noncoding RNAs in failing human heart and remodeling with mechanical circulatory support. Circulation, 129(9), 1009–1021.PubMedPubMedCentral Yang, K. C., Yamada, K. A., Patel, A. Y., Topkara, V. K., George, I., Cheema, F. H., et al. (2014). Deep RNA sequencing reveals dynamic regulation of myocardial noncoding RNAs in failing human heart and remodeling with mechanical circulatory support. Circulation, 129(9), 1009–1021.PubMedPubMedCentral
24.
Zurück zum Zitat Schiano, C., Costa, V., Aprile, M., Grimaldi, V., Maiello, C., Esposito, R., et al. (2017). Heart failure: pilot transcriptomic analysis of cardiac tissue by RNA-sequencing. Cardiol J. Schiano, C., Costa, V., Aprile, M., Grimaldi, V., Maiello, C., Esposito, R., et al. (2017). Heart failure: pilot transcriptomic analysis of cardiac tissue by RNA-sequencing. Cardiol J.
25.
Zurück zum Zitat Zhang, J., Feng, C., Song, C., Ai, B., Bai, X., Liu, Y., et al. (2018). Identification and analysis of a key long non-coding RNAs (lncRNAs)-associated module reveal functional lncRNAs in cardiac hypertrophy. Journal of Cellular and Molecular Medicine, 22(2), 892–903.PubMed Zhang, J., Feng, C., Song, C., Ai, B., Bai, X., Liu, Y., et al. (2018). Identification and analysis of a key long non-coding RNAs (lncRNAs)-associated module reveal functional lncRNAs in cardiac hypertrophy. Journal of Cellular and Molecular Medicine, 22(2), 892–903.PubMed
26.
Zurück zum Zitat Wang, K., Liu, F., Zhou, L. Y., Long, B., Yuan, S. M., Wang, Y., et al. (2014). The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. Circulation Research, 114(9), 1377–1388.PubMed Wang, K., Liu, F., Zhou, L. Y., Long, B., Yuan, S. M., Wang, Y., et al. (2014). The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489. Circulation Research, 114(9), 1377–1388.PubMed
27.
Zurück zum Zitat Zhu, X. H., Yuan, Y. X., Rao, S. L., & Wang, P. (2016). LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150. European Review for Medical and Pharmacological Sciences, 20(17), 3653–3660.PubMed Zhu, X. H., Yuan, Y. X., Rao, S. L., & Wang, P. (2016). LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150. European Review for Medical and Pharmacological Sciences, 20(17), 3653–3660.PubMed
28.
Zurück zum Zitat Lai, Y. J., He, S., Ma, L. M., Lin, H., Ren, B. Y., Ma, J., et al. (2017). HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy. Molecular and Cellular Biochemistry, 432(1–2), 179–187.PubMed Lai, Y. J., He, S., Ma, L. M., Lin, H., Ren, B. Y., Ma, J., et al. (2017). HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy. Molecular and Cellular Biochemistry, 432(1–2), 179–187.PubMed
29.
Zurück zum Zitat Jiang, F., Zhou, X., & Huang, J. (2016). Long non-coding RNA-ROR mediates the reprogramming in cardiac hypertrophy. PLoS One, 11(4), e0152767.PubMedPubMedCentral Jiang, F., Zhou, X., & Huang, J. (2016). Long non-coding RNA-ROR mediates the reprogramming in cardiac hypertrophy. PLoS One, 11(4), e0152767.PubMedPubMedCentral
30.
Zurück zum Zitat Keniry, A., Oxley, D., Monnier, P., Kyba, M., Dandolo, L., Smits, G., et al. (2012). The H19 lincRNA is a developmental reservoir of miR-675 that suppresses growth and lgf1r. Nature Cell Biology, 14(7), 659–665.PubMedPubMedCentral Keniry, A., Oxley, D., Monnier, P., Kyba, M., Dandolo, L., Smits, G., et al. (2012). The H19 lincRNA is a developmental reservoir of miR-675 that suppresses growth and lgf1r. Nature Cell Biology, 14(7), 659–665.PubMedPubMedCentral
31.
Zurück zum Zitat Liu, L. T., An, X. B., Li, Z. H., Song, Y., Li, L. L., Zuo, S., et al. (2016). The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy. Cardiovascular Research, 111(1), 56–65.PubMed Liu, L. T., An, X. B., Li, Z. H., Song, Y., Li, L. L., Zuo, S., et al. (2016). The H19 long noncoding RNA is a novel negative regulator of cardiomyocyte hypertrophy. Cardiovascular Research, 111(1), 56–65.PubMed
32.
Zurück zum Zitat Han, P., Li, W., Lin, C. H., Yang, J., Shang, C., Nuernberg, S. T., et al. (2014). A long noncoding RNA protects the heart from pathological hypertrophy. Nature, 514(7520), 102–106.PubMedPubMedCentral Han, P., Li, W., Lin, C. H., Yang, J., Shang, C., Nuernberg, S. T., et al. (2014). A long noncoding RNA protects the heart from pathological hypertrophy. Nature, 514(7520), 102–106.PubMedPubMedCentral
33.
Zurück zum Zitat Wang, Z., Zhang, X. J., Ji, Y. X., Zhang, P., Deng, K. Q., Gong, J., et al. (2016). The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy. Nature Medicine, 22(10), 1131–1139.PubMedPubMedCentral Wang, Z., Zhang, X. J., Ji, Y. X., Zhang, P., Deng, K. Q., Gong, J., et al. (2016). The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy. Nature Medicine, 22(10), 1131–1139.PubMedPubMedCentral
34.
Zurück zum Zitat Shao, M., Chen, G., Lv, F., Liu, Y., Tian, H., Tao, R., et al. (2017). LncRNA TINCR attenuates cardiac hypertrophy by epigenetically silencing CaMKII. Oncotarget, 8(29), 47565–47573.PubMedPubMedCentral Shao, M., Chen, G., Lv, F., Liu, Y., Tian, H., Tao, R., et al. (2017). LncRNA TINCR attenuates cardiac hypertrophy by epigenetically silencing CaMKII. Oncotarget, 8(29), 47565–47573.PubMedPubMedCentral
35.
Zurück zum Zitat Viereck, J., Kumarswamy, R., Foinquinos, A., Xiao, K., Avramopoulos, P., Kunz, M., et al. (2016). Long noncoding RNA Chast promotes cardiac remodeling. Science Translational Medicine, 8(326), 326ra322. Viereck, J., Kumarswamy, R., Foinquinos, A., Xiao, K., Avramopoulos, P., Kunz, M., et al. (2016). Long noncoding RNA Chast promotes cardiac remodeling. Science Translational Medicine, 8(326), 326ra322.
36.
Zurück zum Zitat Sun, W., Julie Li, Y. S., Huang, H. D., Shyy, J. Y., & Chien, S. (2010). MicroRNA: a master regulator of cellular processes for bioengineering systems. Annual Review of Biomedical Engineering, 12, 1–27.PubMed Sun, W., Julie Li, Y. S., Huang, H. D., Shyy, J. Y., & Chien, S. (2010). MicroRNA: a master regulator of cellular processes for bioengineering systems. Annual Review of Biomedical Engineering, 12, 1–27.PubMed
37.
Zurück zum Zitat Zhao, Y., Ransom, J. F., Li, A., Vedantham, V., von Drehle, M., Muth, A. N., et al. (2007). Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2. Cell, 129(2), 303–317.PubMed Zhao, Y., Ransom, J. F., Li, A., Vedantham, V., von Drehle, M., Muth, A. N., et al. (2007). Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2. Cell, 129(2), 303–317.PubMed
38.
Zurück zum Zitat Zhao, Y., Samal, E., & Srivastava, D. (2005). Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis. Nature, 436(7048), 214–220.PubMed Zhao, Y., Samal, E., & Srivastava, D. (2005). Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis. Nature, 436(7048), 214–220.PubMed
39.
Zurück zum Zitat Chen, J. F., Mandel, E. M., Thomson, J. M., Wu, Q., Callis, T. E., Hammond, S. M., et al. (2006). The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation. Nature Genetics, 38(2), 228–233.PubMed Chen, J. F., Mandel, E. M., Thomson, J. M., Wu, Q., Callis, T. E., Hammond, S. M., et al. (2006). The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation. Nature Genetics, 38(2), 228–233.PubMed
40.
Zurück zum Zitat Yang, B., Lin, H., Xiao, J., Lu, Y., Luo, X., Li, B., et al. (2007). The muscle-specific microRNA miR-1 regulates cardiac arrhythmogenic potential by targeting GJA1 and KCNJ2. Nature Medicine, 13(4), 486–491.PubMed Yang, B., Lin, H., Xiao, J., Lu, Y., Luo, X., Li, B., et al. (2007). The muscle-specific microRNA miR-1 regulates cardiac arrhythmogenic potential by targeting GJA1 and KCNJ2. Nature Medicine, 13(4), 486–491.PubMed
41.
Zurück zum Zitat Sayed, D., Hong, C., Chen, I. Y., Lypowy, J., & Abdellatif, M. (2007). MicroRNAs play an essential role in the development of cardiac hypertrophy. Circulation Research, 100(3), 416–424.PubMed Sayed, D., Hong, C., Chen, I. Y., Lypowy, J., & Abdellatif, M. (2007). MicroRNAs play an essential role in the development of cardiac hypertrophy. Circulation Research, 100(3), 416–424.PubMed
42.
Zurück zum Zitat Ikeda, S., He, A., Kong, S. W., Lu, J., Bejar, R., Bodyak, N., et al. (2009). MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes. Molecular and Cellular Biology, 29(8), 2193–2204.PubMedPubMedCentral Ikeda, S., He, A., Kong, S. W., Lu, J., Bejar, R., Bodyak, N., et al. (2009). MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes. Molecular and Cellular Biology, 29(8), 2193–2204.PubMedPubMedCentral
43.
Zurück zum Zitat Elia, L., Contu, R., Quintavalle, M., Varrone, F., Chimenti, C., Russo, M. A., et al. (2009). Reciprocal regulation of microRNA-1 and insulin-like growth factor-1 signal transduction cascade in cardiac and skeletal muscle in physiological and pathological conditions. Circulation, 120(23), 2377–2385.PubMedPubMedCentral Elia, L., Contu, R., Quintavalle, M., Varrone, F., Chimenti, C., Russo, M. A., et al. (2009). Reciprocal regulation of microRNA-1 and insulin-like growth factor-1 signal transduction cascade in cardiac and skeletal muscle in physiological and pathological conditions. Circulation, 120(23), 2377–2385.PubMedPubMedCentral
44.
Zurück zum Zitat Li, Q., Song, X. W., Zou, J., Wang, G. K., Kremneva, E., Li, X. Q., et al. (2010). Attenuation of microRNA-1 derepresses the cytoskeleton regulatory protein twinfilin-1 to provoke cardiac hypertrophy. Journal of Cell Science, 123(Pt 14), 2444–2452.PubMed Li, Q., Song, X. W., Zou, J., Wang, G. K., Kremneva, E., Li, X. Q., et al. (2010). Attenuation of microRNA-1 derepresses the cytoskeleton regulatory protein twinfilin-1 to provoke cardiac hypertrophy. Journal of Cell Science, 123(Pt 14), 2444–2452.PubMed
45.
Zurück zum Zitat Yuan, W., Tang, C., Zhu, W., Zhu, J., Lin, Q., Fu, Y., et al. (2016). CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy. Molecular and Cellular Biochemistry, 412(1–2), 289–296.PubMed Yuan, W., Tang, C., Zhu, W., Zhu, J., Lin, Q., Fu, Y., et al. (2016). CDK6 mediates the effect of attenuation of miR-1 on provoking cardiomyocyte hypertrophy. Molecular and Cellular Biochemistry, 412(1–2), 289–296.PubMed
46.
Zurück zum Zitat Karakikes, I., Chaanine, A. H., Kang, S., Mukete, B. N., Jeong, D., Zhang, S., et al. (2013). Therapeutic cardiac-targeted delivery of miR-1 reverses pressure overload-induced cardiac hypertrophy and attenuates pathological remodeling. Journal of the American Heart Association, 2(2), e000078.PubMedPubMedCentral Karakikes, I., Chaanine, A. H., Kang, S., Mukete, B. N., Jeong, D., Zhang, S., et al. (2013). Therapeutic cardiac-targeted delivery of miR-1 reverses pressure overload-induced cardiac hypertrophy and attenuates pathological remodeling. Journal of the American Heart Association, 2(2), e000078.PubMedPubMedCentral
47.
Zurück zum Zitat Liu, N., Williams, A. H., Kim, Y., McAnally, J., Bezprozvannaya, S., Sutherland, L. B., et al. (2007). An intragenic MEF2-dependent enhancer directs muscle-specific expression of microRNAs 1 and 133. Proceedings of the National Academy of Sciences of the United States of America, 104(52), 20844–20849.PubMedPubMedCentral Liu, N., Williams, A. H., Kim, Y., McAnally, J., Bezprozvannaya, S., Sutherland, L. B., et al. (2007). An intragenic MEF2-dependent enhancer directs muscle-specific expression of microRNAs 1 and 133. Proceedings of the National Academy of Sciences of the United States of America, 104(52), 20844–20849.PubMedPubMedCentral
48.
Zurück zum Zitat McCarthy, J. J. (2008). MicroRNA-206: the skeletal muscle-specific myomiR. Biochimica et Biophysica Acta, 1779(11), 682–691.PubMedPubMedCentral McCarthy, J. J. (2008). MicroRNA-206: the skeletal muscle-specific myomiR. Biochimica et Biophysica Acta, 1779(11), 682–691.PubMedPubMedCentral
49.
Zurück zum Zitat Care, A., Catalucci, D., Felicetti, F., Bonci, D., Addario, A., Gallo, P., et al. (2007). MicroRNA-133 controls cardiac hypertrophy. Nature Medicine, 13(5), 613–618.PubMed Care, A., Catalucci, D., Felicetti, F., Bonci, D., Addario, A., Gallo, P., et al. (2007). MicroRNA-133 controls cardiac hypertrophy. Nature Medicine, 13(5), 613–618.PubMed
50.
Zurück zum Zitat Liu, N., Bezprozvannaya, S., Williams, A. H., Qi, X., Richardson, J. A., Bassel-Duby, R., et al. (2008). microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart. Genes & Development, 22(23), 3242–3254. Liu, N., Bezprozvannaya, S., Williams, A. H., Qi, X., Richardson, J. A., Bassel-Duby, R., et al. (2008). microRNA-133a regulates cardiomyocyte proliferation and suppresses smooth muscle gene expression in the heart. Genes & Development, 22(23), 3242–3254.
51.
Zurück zum Zitat Luo, X., Lin, H., Pan, Z., Xiao, J., Zhang, Y., Lu, Y., et al. (2008). Down-regulation of miR-1/miR-133 contributes to re-expression of pacemaker channel genes HCN2 and HCN4 in hypertrophic heart. The Journal of Biological Chemistry, 283(29), 20045–20052.PubMed Luo, X., Lin, H., Pan, Z., Xiao, J., Zhang, Y., Lu, Y., et al. (2008). Down-regulation of miR-1/miR-133 contributes to re-expression of pacemaker channel genes HCN2 and HCN4 in hypertrophic heart. The Journal of Biological Chemistry, 283(29), 20045–20052.PubMed
52.
Zurück zum Zitat Dong, D. L., Chen, C., Huo, R., Wang, N., Li, Z., Tu, Y. J., et al. (2010). Reciprocal repression between microRNA-133 and calcineurin regulates cardiac hypertrophy: a novel mechanism for progressive cardiac hypertrophy. Hypertension, 55(4), 946–952.PubMed Dong, D. L., Chen, C., Huo, R., Wang, N., Li, Z., Tu, Y. J., et al. (2010). Reciprocal repression between microRNA-133 and calcineurin regulates cardiac hypertrophy: a novel mechanism for progressive cardiac hypertrophy. Hypertension, 55(4), 946–952.PubMed
53.
Zurück zum Zitat Li, Q., Lin, X., Yang, X., & Chang, J. (2010). NFATc4 is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression. American Journal of Physiology. Heart and Circulatory Physiology, 298(5), H1340–H1347.PubMedPubMedCentral Li, Q., Lin, X., Yang, X., & Chang, J. (2010). NFATc4 is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression. American Journal of Physiology. Heart and Circulatory Physiology, 298(5), H1340–H1347.PubMedPubMedCentral
54.
Zurück zum Zitat Han, M., Yang, Z., Sayed, D., He, M., Gao, S., Lin, L., et al. (2012). GATA4 expression is primarily regulated via a miR-26b-dependent post-transcriptional mechanism during cardiac hypertrophy. Cardiovascular Research, 93(4), 645–654.PubMedPubMedCentral Han, M., Yang, Z., Sayed, D., He, M., Gao, S., Lin, L., et al. (2012). GATA4 expression is primarily regulated via a miR-26b-dependent post-transcriptional mechanism during cardiac hypertrophy. Cardiovascular Research, 93(4), 645–654.PubMedPubMedCentral
55.
Zurück zum Zitat Li, R., Yan, G., Zhang, Q., Jiang, Y., Sun, H., Hu, Y., et al. (2013). miR-145 inhibits isoproterenol-induced cardiomyocyte hypertrophy by targeting the expression and localization of GATA6. FEBS Letters, 587(12), 1754–1761.PubMedPubMedCentral Li, R., Yan, G., Zhang, Q., Jiang, Y., Sun, H., Hu, Y., et al. (2013). miR-145 inhibits isoproterenol-induced cardiomyocyte hypertrophy by targeting the expression and localization of GATA6. FEBS Letters, 587(12), 1754–1761.PubMedPubMedCentral
56.
Zurück zum Zitat Ganesan, J., Ramanujam, D., Sassi, Y., Ahles, A., Jentzsch, C., Werfel, S., et al. (2013). MiR-378 controls cardiac hypertrophy by combined repression of mitogen-activated protein kinase pathway factors. Circulation, 127(21), 2097–2106.PubMed Ganesan, J., Ramanujam, D., Sassi, Y., Ahles, A., Jentzsch, C., Werfel, S., et al. (2013). MiR-378 controls cardiac hypertrophy by combined repression of mitogen-activated protein kinase pathway factors. Circulation, 127(21), 2097–2106.PubMed
57.
Zurück zum Zitat Wang, Y. S., Zhou, J., Hong, K., Cheng, X. S., & Li, Y. G. (2015). MicroRNA-223 displays a protective role against cardiomyocyte hypertrophy by targeting cardiac troponin I-interacting kinase. Cellular Physiology and Biochemistry, 35(4), 1546–1556.PubMed Wang, Y. S., Zhou, J., Hong, K., Cheng, X. S., & Li, Y. G. (2015). MicroRNA-223 displays a protective role against cardiomyocyte hypertrophy by targeting cardiac troponin I-interacting kinase. Cellular Physiology and Biochemistry, 35(4), 1546–1556.PubMed
58.
Zurück zum Zitat Lee, J. S., Yang, D. K., Park, J. H., Kim, J. O., Park, W. J., Cho, C., et al. (2017). MicroRNA-101b attenuates cardiomyocyte hypertrophy by inhibiting protein kinase C epsilon signaling. FEBS Letters, 591(1), 16–27.PubMed Lee, J. S., Yang, D. K., Park, J. H., Kim, J. O., Park, W. J., Cho, C., et al. (2017). MicroRNA-101b attenuates cardiomyocyte hypertrophy by inhibiting protein kinase C epsilon signaling. FEBS Letters, 591(1), 16–27.PubMed
59.
Zurück zum Zitat Duan, Q., Chen, C., Yang, L., Li, N., Gong, W., Li, S., et al. (2015). MicroRNA regulation of unfolded protein response transcription factor XBP1 in the progression of cardiac hypertrophy and heart failure in vivo. Journal of Translational Medicine, 13, 363.PubMedPubMedCentral Duan, Q., Chen, C., Yang, L., Li, N., Gong, W., Li, S., et al. (2015). MicroRNA regulation of unfolded protein response transcription factor XBP1 in the progression of cardiac hypertrophy and heart failure in vivo. Journal of Translational Medicine, 13, 363.PubMedPubMedCentral
60.
Zurück zum Zitat Yang, Y., Ago, T., Zhai, P., Abdellatif, M., & Sadoshima, J. (2011). Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7. Circulation Research, 108(3), 305–313.PubMed Yang, Y., Ago, T., Zhai, P., Abdellatif, M., & Sadoshima, J. (2011). Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7. Circulation Research, 108(3), 305–313.PubMed
61.
Zurück zum Zitat Huang, J., Sun, W., Huang, H., Ye, J., Pan, W., Zhong, Y., et al. (2014). miR-34a modulates angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity. PLoS One, 9(4), e94382.PubMedPubMedCentral Huang, J., Sun, W., Huang, H., Ye, J., Pan, W., Zhong, Y., et al. (2014). miR-34a modulates angiotensin II-induced myocardial hypertrophy by direct inhibition of ATG9A expression and autophagic activity. PLoS One, 9(4), e94382.PubMedPubMedCentral
62.
Zurück zum Zitat Pan, W., Zhong, Y., Cheng, C., Liu, B., Wang, L., Li, A., et al. (2013). MiR-30-regulated autophagy mediates angiotensin II-induced myocardial hypertrophy. PLoS One, 8(1), e53950.PubMedPubMedCentral Pan, W., Zhong, Y., Cheng, C., Liu, B., Wang, L., Li, A., et al. (2013). MiR-30-regulated autophagy mediates angiotensin II-induced myocardial hypertrophy. PLoS One, 8(1), e53950.PubMedPubMedCentral
63.
Zurück zum Zitat Yan, M., Chen, C., Gong, W., Yin, Z., Zhou, L., Chaugai, S., et al. (2015). miR-21-3p regulates cardiac hypertrophic response by targeting histone deacetylase-8. Cardiovascular Research, 105(3), 340–352.PubMed Yan, M., Chen, C., Gong, W., Yin, Z., Zhou, L., Chaugai, S., et al. (2015). miR-21-3p regulates cardiac hypertrophic response by targeting histone deacetylase-8. Cardiovascular Research, 105(3), 340–352.PubMed
64.
Zurück zum Zitat Wang, K., Long, B., Zhou, J., & Li, P. F. (2010). miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy. The Journal of Biological Chemistry, 285(16), 11903–11912.PubMedPubMedCentral Wang, K., Long, B., Zhou, J., & Li, P. F. (2010). miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy. The Journal of Biological Chemistry, 285(16), 11903–11912.PubMedPubMedCentral
65.
Zurück zum Zitat Kim, J. O., Song, D. W., Kwon, E. J., Hong, S. E., Song, H. K., Min, C. K., et al. (2015). miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways. PLoS One, 10(3), e0122509.PubMedPubMedCentral Kim, J. O., Song, D. W., Kwon, E. J., Hong, S. E., Song, H. K., Min, C. K., et al. (2015). miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways. PLoS One, 10(3), e0122509.PubMedPubMedCentral
66.
Zurück zum Zitat van Rooij, E., Sutherland, L. B., Liu, N., Williams, A. H., McAnally, J., Gerard, R. D., et al. (2006). A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure. Proceedings of the National Academy of Sciences of the United States of America, 103(48), 18255–18260.PubMedPubMedCentral van Rooij, E., Sutherland, L. B., Liu, N., Williams, A. H., McAnally, J., Gerard, R. D., et al. (2006). A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure. Proceedings of the National Academy of Sciences of the United States of America, 103(48), 18255–18260.PubMedPubMedCentral
68.
Zurück zum Zitat Callis, T. E., Pandya, K., Seok, H. Y., Tang, R. H., Tatsuguchi, M., Huang, Z. P., et al. (2009). MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. The Journal of Clinical Investigation, 119(9), 2772–2786.PubMedPubMedCentral Callis, T. E., Pandya, K., Seok, H. Y., Tang, R. H., Tatsuguchi, M., Huang, Z. P., et al. (2009). MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. The Journal of Clinical Investigation, 119(9), 2772–2786.PubMedPubMedCentral
69.
Zurück zum Zitat Bernardo, B. C., Gao, X. M., Winbanks, C. E., Boey, E. J., Tham, Y. K., Kiriazis, H., et al. (2012). Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart function. Proceedings of the National Academy of Sciences of the United States of America, 109(43), 17615–17620.PubMedPubMedCentral Bernardo, B. C., Gao, X. M., Winbanks, C. E., Boey, E. J., Tham, Y. K., Kiriazis, H., et al. (2012). Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart function. Proceedings of the National Academy of Sciences of the United States of America, 109(43), 17615–17620.PubMedPubMedCentral
70.
Zurück zum Zitat Bang, C., Batkai, S., Dangwal, S., Gupta, S. K., Foinquinos, A., Holzmann, A., et al. (2014). Cardiac fibroblast-derived microRNA passenger strand-enriched exosomes mediate cardiomyocyte hypertrophy. The Journal of Clinical Investigation, 124(5), 2136–2146.PubMedPubMedCentral Bang, C., Batkai, S., Dangwal, S., Gupta, S. K., Foinquinos, A., Holzmann, A., et al. (2014). Cardiac fibroblast-derived microRNA passenger strand-enriched exosomes mediate cardiomyocyte hypertrophy. The Journal of Clinical Investigation, 124(5), 2136–2146.PubMedPubMedCentral
71.
Zurück zum Zitat da Costa Martins, P. A., Salic, K., Gladka, M. M., Armand, A. S., Leptidis, S., el Azzouzi, H., et al. (2010). MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling. Nature Cell Biology, 12(12), 1220–1227.PubMed da Costa Martins, P. A., Salic, K., Gladka, M. M., Armand, A. S., Leptidis, S., el Azzouzi, H., et al. (2010). MicroRNA-199b targets the nuclear kinase Dyrk1a in an auto-amplification loop promoting calcineurin/NFAT signalling. Nature Cell Biology, 12(12), 1220–1227.PubMed
72.
Zurück zum Zitat Wang, J., Song, Y., Zhang, Y., Xiao, H., Sun, Q., Hou, N., et al. (2012). Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice. Cell Research, 22(3), 516–527.PubMed Wang, J., Song, Y., Zhang, Y., Xiao, H., Sun, Q., Hou, N., et al. (2012). Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice. Cell Research, 22(3), 516–527.PubMed
73.
Zurück zum Zitat Wang, K., Lin, Z. Q., Long, B., Li, J. H., Zhou, J., & Li, P. F. (2012). Cardiac hypertrophy is positively regulated by microRNA miR-23a. The Journal of Biological Chemistry, 287(1), 589–599.PubMed Wang, K., Lin, Z. Q., Long, B., Li, J. H., Zhou, J., & Li, P. F. (2012). Cardiac hypertrophy is positively regulated by microRNA miR-23a. The Journal of Biological Chemistry, 287(1), 589–599.PubMed
74.
Zurück zum Zitat Yang, J., Nie, Y., Wang, F., Hou, J., Cong, X., Hu, S., et al. (2013). Reciprocal regulation of miR-23a and lysophosphatidic acid receptor signaling in cardiomyocyte hypertrophy. Biochimica et Biophysica Acta, 1831(8), 1386–1394.PubMed Yang, J., Nie, Y., Wang, F., Hou, J., Cong, X., Hu, S., et al. (2013). Reciprocal regulation of miR-23a and lysophosphatidic acid receptor signaling in cardiomyocyte hypertrophy. Biochimica et Biophysica Acta, 1831(8), 1386–1394.PubMed
75.
Zurück zum Zitat Ucar, A., Gupta, S. K., Fiedler, J., Erikci, E., Kardasinski, M., Batkai, S., et al. (2012). The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. Nature Communications, 3, 1078.PubMedPubMedCentral Ucar, A., Gupta, S. K., Fiedler, J., Erikci, E., Kardasinski, M., Batkai, S., et al. (2012). The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy. Nature Communications, 3, 1078.PubMedPubMedCentral
76.
Zurück zum Zitat Wang, C., Wang, S., Zhao, P., Wang, X., Wang, J., Wang, Y., et al. (2012). MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression. Journal of Cellular Biochemistry, 113(6), 2040–2046.PubMed Wang, C., Wang, S., Zhao, P., Wang, X., Wang, J., Wang, Y., et al. (2012). MiR-221 promotes cardiac hypertrophy in vitro through the modulation of p27 expression. Journal of Cellular Biochemistry, 113(6), 2040–2046.PubMed
77.
Zurück zum Zitat Ge, Y., Pan, S., Guan, D., Yin, H., Fan, Y., Liu, J., et al. (2013). MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways. Biochimica et Biophysica Acta, 1832(1), 1–10.PubMed Ge, Y., Pan, S., Guan, D., Yin, H., Fan, Y., Liu, J., et al. (2013). MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways. Biochimica et Biophysica Acta, 1832(1), 1–10.PubMed
78.
Zurück zum Zitat Huang, Z. P., Chen, J., Seok, H. Y., Zhang, Z., Kataoka, M., Hu, X., et al. (2013). MicroRNA-22 regulates cardiac hypertrophy and remodeling in response to stress. Circulation Research, 112(9), 1234–1243.PubMedPubMedCentral Huang, Z. P., Chen, J., Seok, H. Y., Zhang, Z., Kataoka, M., Hu, X., et al. (2013). MicroRNA-22 regulates cardiac hypertrophy and remodeling in response to stress. Circulation Research, 112(9), 1234–1243.PubMedPubMedCentral
79.
Zurück zum Zitat Li, C., Li, X., Gao, X., Zhang, R., Zhang, Y., Liang, H., et al. (2014). MicroRNA-328 as a regulator of cardiac hypertrophy. International Journal of Cardiology, 173(2), 268–276.PubMed Li, C., Li, X., Gao, X., Zhang, R., Zhang, Y., Liang, H., et al. (2014). MicroRNA-328 as a regulator of cardiac hypertrophy. International Journal of Cardiology, 173(2), 268–276.PubMed
80.
Zurück zum Zitat He, W., Huang, H., Xie, Q., Wang, Z., Fan, Y., Kong, B., et al. (2016). MiR-155 knockout in fibroblasts improves cardiac remodeling by targeting tumor protein p53-inducible nuclear protein 1. Journal of Cardiovascular Pharmacology and Therapeutics, 21(4), 423–435.PubMed He, W., Huang, H., Xie, Q., Wang, Z., Fan, Y., Kong, B., et al. (2016). MiR-155 knockout in fibroblasts improves cardiac remodeling by targeting tumor protein p53-inducible nuclear protein 1. Journal of Cardiovascular Pharmacology and Therapeutics, 21(4), 423–435.PubMed
81.
Zurück zum Zitat Sanger, H. L., Klotz, G., Riesner, D., Gross, H. J., & Kleinschmidt, A. K. (1976). Viroids are single-stranded covalently closed circular RNA molecules existing as highly base-paired rod-like structures. Proceedings of the National Academy of Sciences of the United States of America, 73(11), 3852–3856.PubMedPubMedCentral Sanger, H. L., Klotz, G., Riesner, D., Gross, H. J., & Kleinschmidt, A. K. (1976). Viroids are single-stranded covalently closed circular RNA molecules existing as highly base-paired rod-like structures. Proceedings of the National Academy of Sciences of the United States of America, 73(11), 3852–3856.PubMedPubMedCentral
82.
Zurück zum Zitat Szabo, L., & Salzman, J. (2016). Detecting circular RNAs: bioinformatic and experimental challenges. Nature Reviews. Genetics, 17(11), 679–692.PubMedPubMedCentral Szabo, L., & Salzman, J. (2016). Detecting circular RNAs: bioinformatic and experimental challenges. Nature Reviews. Genetics, 17(11), 679–692.PubMedPubMedCentral
83.
Zurück zum Zitat Qu, S., Zhong, Y., Shang, R., Zhang, X., Song, W., Kjems, J., et al. (2016). The emerging landscape of circular RNA in life processes. RNA Biol, 1–8. Qu, S., Zhong, Y., Shang, R., Zhang, X., Song, W., Kjems, J., et al. (2016). The emerging landscape of circular RNA in life processes. RNA Biol, 1–8.
84.
Zurück zum Zitat Zheng, Q., Bao, C., Guo, W., Li, S., Chen, J., Chen, B., et al. (2016). Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs. Nature Communications, 7, 11215.PubMedPubMedCentral Zheng, Q., Bao, C., Guo, W., Li, S., Chen, J., Chen, B., et al. (2016). Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs. Nature Communications, 7, 11215.PubMedPubMedCentral
85.
Zurück zum Zitat Wang, K., Long, B., Liu, F., Wang, J. X., Liu, C. Y., Zhao, B., et al. (2016). A circular RNA protects the heart from pathological hypertrophy and heart failure by targeting miR-223. European Heart Journal, 37(33), 2602–2611.PubMed Wang, K., Long, B., Liu, F., Wang, J. X., Liu, C. Y., Zhao, B., et al. (2016). A circular RNA protects the heart from pathological hypertrophy and heart failure by targeting miR-223. European Heart Journal, 37(33), 2602–2611.PubMed
86.
Zurück zum Zitat Jakobi, T., Czaja-Hasse, L. F., Reinhardt, R., & Dieterich, C. (2016). Profiling and validation of the circular RNA repertoire in adult murine hearts. Genomics, Proteomics & Bioinformatics, 14(4), 216–223. Jakobi, T., Czaja-Hasse, L. F., Reinhardt, R., & Dieterich, C. (2016). Profiling and validation of the circular RNA repertoire in adult murine hearts. Genomics, Proteomics & Bioinformatics, 14(4), 216–223.
87.
Zurück zum Zitat Khan, M. A., Reckman, Y. J., Aufiero, S., van den Hoogenhof, M. M., van der Made, I., Beqqali, A., et al. (2016). RBM20 regulates circular RNA production from the Titin gene. Circulation Research, 119(9), 996–1003.PubMed Khan, M. A., Reckman, Y. J., Aufiero, S., van den Hoogenhof, M. M., van der Made, I., Beqqali, A., et al. (2016). RBM20 regulates circular RNA production from the Titin gene. Circulation Research, 119(9), 996–1003.PubMed
88.
Zurück zum Zitat Werfel, S., Nothjunge, S., Schwarzmayr, T., Strom, T. M., Meitinger, T., & Engelhardt, S. (2016). Characterization of circular RNAs in human, mouse and rat hearts. Journal of Molecular and Cellular Cardiology, 98, 103–107.PubMed Werfel, S., Nothjunge, S., Schwarzmayr, T., Strom, T. M., Meitinger, T., & Engelhardt, S. (2016). Characterization of circular RNAs in human, mouse and rat hearts. Journal of Molecular and Cellular Cardiology, 98, 103–107.PubMed
89.
Zurück zum Zitat Tan, W. L., Lim, B. T., Anene-Nzelu, C. G., Ackers-Johnson, M., Dashi, A., See, K., et al. (2017). A landscape of circular RNA expression in the human heart. Cardiovascular Research, 113(3), 298–309.PubMed Tan, W. L., Lim, B. T., Anene-Nzelu, C. G., Ackers-Johnson, M., Dashi, A., See, K., et al. (2017). A landscape of circular RNA expression in the human heart. Cardiovascular Research, 113(3), 298–309.PubMed
90.
Zurück zum Zitat Fernandes, T., Hashimoto, N. Y., Magalhaes, F. C., Fernandes, F. B., Casarini, D. E., Carmona, A. K., et al. (2011). Aerobic exercise training-induced left ventricular hypertrophy involves regulatory microRNAs, decreased angiotensin-converting enzyme-angiotensin II, and synergistic regulation of angiotensin-converting enzyme 2-angiotensin (1-7). Hypertension, 58(2), 182–189.PubMedPubMedCentral Fernandes, T., Hashimoto, N. Y., Magalhaes, F. C., Fernandes, F. B., Casarini, D. E., Carmona, A. K., et al. (2011). Aerobic exercise training-induced left ventricular hypertrophy involves regulatory microRNAs, decreased angiotensin-converting enzyme-angiotensin II, and synergistic regulation of angiotensin-converting enzyme 2-angiotensin (1-7). Hypertension, 58(2), 182–189.PubMedPubMedCentral
91.
Zurück zum Zitat Ramasamy, S., Velmurugan, G., Shanmugha Rajan, K., Ramprasath, T., & Kalpana, K. (2015). MiRNAs with apoptosis regulating potential are differentially expressed in chronic exercise-induced physiologically hypertrophied hearts. PLoS One, 10(3), e0121401.PubMedPubMedCentral Ramasamy, S., Velmurugan, G., Shanmugha Rajan, K., Ramprasath, T., & Kalpana, K. (2015). MiRNAs with apoptosis regulating potential are differentially expressed in chronic exercise-induced physiologically hypertrophied hearts. PLoS One, 10(3), e0121401.PubMedPubMedCentral
92.
Zurück zum Zitat Ma, Z., Qi, J., Meng, S., Wen, B., & Zhang, J. (2013). Swimming exercise training-induced left ventricular hypertrophy involves microRNAs and synergistic regulation of the PI3K/AKT/mTOR signaling pathway. European Journal of Applied Physiology, 113(10), 2473–2486.PubMed Ma, Z., Qi, J., Meng, S., Wen, B., & Zhang, J. (2013). Swimming exercise training-induced left ventricular hypertrophy involves microRNAs and synergistic regulation of the PI3K/AKT/mTOR signaling pathway. European Journal of Applied Physiology, 113(10), 2473–2486.PubMed
93.
Zurück zum Zitat Soci, U. P., Fernandes, T., Hashimoto, N. Y., Mota, G. F., Amadeu, M. A., Rosa, K. T., et al. (2011). MicroRNAs 29 are involved in the improvement of ventricular compliance promoted by aerobic exercise training in rats. Physiological Genomics, 43(11), 665–673.PubMedPubMedCentral Soci, U. P., Fernandes, T., Hashimoto, N. Y., Mota, G. F., Amadeu, M. A., Rosa, K. T., et al. (2011). MicroRNAs 29 are involved in the improvement of ventricular compliance promoted by aerobic exercise training in rats. Physiological Genomics, 43(11), 665–673.PubMedPubMedCentral
94.
Zurück zum Zitat Martinelli, N. C., Cohen, C. R., Santos, K. G., Castro, M. A., Biolo, A., Frick, L., et al. (2014). An analysis of the global expression of microRNAs in an experimental model of physiological left ventricular hypertrophy. PLoS One, 9(4), e93271.PubMedPubMedCentral Martinelli, N. C., Cohen, C. R., Santos, K. G., Castro, M. A., Biolo, A., Frick, L., et al. (2014). An analysis of the global expression of microRNAs in an experimental model of physiological left ventricular hypertrophy. PLoS One, 9(4), e93271.PubMedPubMedCentral
95.
Zurück zum Zitat Liu, X., Xiao, J., Zhu, H., Wei, X., Platt, C., Damilano, F., et al. (2015). miR-222 is necessary for exercise-induced cardiac growth and protects against pathological cardiac remodeling. Cell Metabolism, 21(4), 584–595.PubMedPubMedCentral Liu, X., Xiao, J., Zhu, H., Wei, X., Platt, C., Damilano, F., et al. (2015). miR-222 is necessary for exercise-induced cardiac growth and protects against pathological cardiac remodeling. Cell Metabolism, 21(4), 584–595.PubMedPubMedCentral
96.
Zurück zum Zitat Shi, J., Bei, Y., Kong, X., Liu, X., Lei, Z., Xu, T., et al. (2017). miR-17-3p contributes to exercise-induced cardiac growth and protects against myocardial ischemia-reperfusion injury. Theranostics, 7(3), 664–676.PubMedPubMedCentral Shi, J., Bei, Y., Kong, X., Liu, X., Lei, Z., Xu, T., et al. (2017). miR-17-3p contributes to exercise-induced cardiac growth and protects against myocardial ischemia-reperfusion injury. Theranostics, 7(3), 664–676.PubMedPubMedCentral
97.
Zurück zum Zitat Li, Z., Liu, L., Hou, N., Song, Y., An, X., Zhang, Y., et al. (2016). miR-199-sponge transgenic mice develop physiological cardiac hypertrophy. Cardiovascular Research, 110(2), 258–267.PubMed Li, Z., Liu, L., Hou, N., Song, Y., An, X., Zhang, Y., et al. (2016). miR-199-sponge transgenic mice develop physiological cardiac hypertrophy. Cardiovascular Research, 110(2), 258–267.PubMed
98.
Zurück zum Zitat Yang, L., Li, Y., Wang, X., Mu, X., Qin, D., Huang, W., et al. (2016). Overexpression of miR-223 tips the balance of pro- and anti-hypertrophic signaling cascades toward physiologic cardiac hypertrophy. The Journal of Biological Chemistry, 291(30), 15700–15713.PubMedPubMedCentral Yang, L., Li, Y., Wang, X., Mu, X., Qin, D., Huang, W., et al. (2016). Overexpression of miR-223 tips the balance of pro- and anti-hypertrophic signaling cascades toward physiologic cardiac hypertrophy. The Journal of Biological Chemistry, 291(30), 15700–15713.PubMedPubMedCentral
Metadaten
Titel
Noncoding RNAs in Cardiac Hypertrophy
verfasst von
Yongqin Li
Yajun Liang
Yujiao Zhu
Yuhui Zhang
Yihua Bei
Publikationsdatum
31.08.2018
Verlag
Springer US
Erschienen in
Journal of Cardiovascular Translational Research / Ausgabe 6/2018
Print ISSN: 1937-5387
Elektronische ISSN: 1937-5395
DOI
https://doi.org/10.1007/s12265-018-9797-x

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