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Erschienen in: Journal of Cardiovascular Translational Research 6/2012

01.12.2012

Crosstalk Between the Renin–Angiotensin System and the Advance Glycation End Product Axis in the Heart: Role of the Cardiac Fibroblast

verfasst von: Katrina Go Yamazaki, Eileen Gonzalez, Alexander C. Zambon

Erschienen in: Journal of Cardiovascular Translational Research | Ausgabe 6/2012

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Abstract

Cardiac fibroblasts (CFs) are involved in maintaining extracellular matrix (ECM) homeostasis in the heart. CFs mediate responses to hormonal and mechanical stimuli and relay these to other local cell types through release of autocrine and/or paracrine factors. CFs also play important roles in the setting of injury, i.e., myocardial infarction, where ECM production is key to efficient scarring. However, conditions exist in which excess production of ECM by CFs can lead to cardiac fibrosis. Two important pathways known to be involved in development of cardiac fibrosis are renin–angiotensin system (RAS) and advanced glycation end products (AGE) receptor (RAGE) signaling cascades. This report summarizes actions of these two pathways on function of CFs. Because cardiac fibrosis is an important component of diabetic cardiomyopathy, we include new data that suggests a possible crosstalk between the RAS and AGE/RAGE pathway in order to activate CFs in diabetes.
Literatur
1.
Zurück zum Zitat Carey, R. M., & Siragy, H. M. (2003). Newly recognized components of the renin–angiotensin system: Potential roles in cardiovascular and renal regulation. Endocrine Reviews, 24(3), 261–271.PubMedCrossRef Carey, R. M., & Siragy, H. M. (2003). Newly recognized components of the renin–angiotensin system: Potential roles in cardiovascular and renal regulation. Endocrine Reviews, 24(3), 261–271.PubMedCrossRef
2.
Zurück zum Zitat Unger, T., Paulis, L., & Sica, D. A. Therapeutic perspectives in hypertension: Novel means for renin–angiotensin–aldosterone system modulation and emerging device-based approaches. European Heart Journal, 32(22), 2739–2747. doi:10.1093/eurheartj/ehr253. Unger, T., Paulis, L., & Sica, D. A. Therapeutic perspectives in hypertension: Novel means for renin–angiotensin–aldosterone system modulation and emerging device-based approaches. European Heart Journal, 32(22), 2739–2747. doi:10.​1093/​eurheartj/​ehr253.
4.
Zurück zum Zitat Ma, T. K., Kam, K. K., Yan, B. P., & Lam, Y. Y. Renin–angiotensin–aldosterone system blockade for cardiovascular diseases: Current status. British Journal of Pharmacology, 160(6), 1273–1292. doi:10.1111/j.1476-5381.2010.00750.x. Ma, T. K., Kam, K. K., Yan, B. P., & Lam, Y. Y. Renin–angiotensin–aldosterone system blockade for cardiovascular diseases: Current status. British Journal of Pharmacology, 160(6), 1273–1292. doi:10.​1111/​j.​1476-5381.​2010.​00750.​x.
5.
Zurück zum Zitat Dostal, D. E., & Baker, K. M. (1999). The cardiac renin–angiotensin system: Conceptual, or a regulator of cardiac function? Circulation Research, 85(7), 643–650.PubMedCrossRef Dostal, D. E., & Baker, K. M. (1999). The cardiac renin–angiotensin system: Conceptual, or a regulator of cardiac function? Circulation Research, 85(7), 643–650.PubMedCrossRef
6.
Zurück zum Zitat Gray, M. O., Long, C. S., Kalinyak, J. E., Li, H. T., & Karliner, J. S. (1998). Angiotensin II stimulates cardiac myocyte hypertrophy via paracrine release of TGF-beta 1 and endothelin-1 from fibroblasts. Cardiovascular Research, 40(2), 352–363.PubMedCrossRef Gray, M. O., Long, C. S., Kalinyak, J. E., Li, H. T., & Karliner, J. S. (1998). Angiotensin II stimulates cardiac myocyte hypertrophy via paracrine release of TGF-beta 1 and endothelin-1 from fibroblasts. Cardiovascular Research, 40(2), 352–363.PubMedCrossRef
7.
Zurück zum Zitat Buhler, F. R., Bolli, P., Kiowski, W., Erne, P., Hulthen, U. L., & Block, L. H. (1984). Renin profiling to select antihypertensive baseline drugs. Renin inhibitors for high-renin and calcium entry blockers for low-renin patients. American Journal of Medicine, 77(2A), 36–42.PubMed Buhler, F. R., Bolli, P., Kiowski, W., Erne, P., Hulthen, U. L., & Block, L. H. (1984). Renin profiling to select antihypertensive baseline drugs. Renin inhibitors for high-renin and calcium entry blockers for low-renin patients. American Journal of Medicine, 77(2A), 36–42.PubMed
8.
Zurück zum Zitat Weiss, D., Sorescu, D., & Taylor, W. R. (2001). Angiotensin II and atherosclerosis. The American Journal of Cardiology, 87(8A), 25C–32C.PubMedCrossRef Weiss, D., Sorescu, D., & Taylor, W. R. (2001). Angiotensin II and atherosclerosis. The American Journal of Cardiology, 87(8A), 25C–32C.PubMedCrossRef
9.
Zurück zum Zitat Weiss, D., Kools, J. J., & Taylor, W. R. (2001). Angiotensin II-induced hypertension accelerates the development of atherosclerosis in apoE-deficient mice. Circulation, 103(3), 448–454.PubMedCrossRef Weiss, D., Kools, J. J., & Taylor, W. R. (2001). Angiotensin II-induced hypertension accelerates the development of atherosclerosis in apoE-deficient mice. Circulation, 103(3), 448–454.PubMedCrossRef
11.
Zurück zum Zitat Iwata, M., Cowling, R. T., Yeo, S. J., & Greenberg, B. Targeting the ACE2–Ang-(1–7) pathway in cardiac fibroblasts to treat cardiac remodeling and heart failure. Journal of Molecular and Cellular Cardiology, 51(4), 542–547. doi:10.1016/j.yjmcc.2010.12.003. Iwata, M., Cowling, R. T., Yeo, S. J., & Greenberg, B. Targeting the ACE2–Ang-(1–7) pathway in cardiac fibroblasts to treat cardiac remodeling and heart failure. Journal of Molecular and Cellular Cardiology, 51(4), 542–547. doi:10.​1016/​j.​yjmcc.​2010.​12.​003.
12.
Zurück zum Zitat Singh, V. P., Baker, K. M., & Kumar, R. (2008). Activation of the intracellular renin–angiotensin system in cardiac fibroblasts by high glucose: Role in extracellular matrix production. American Journal of Physiology. Heart and Circulatory Physiology, 294(4), H1675–H1684. doi:10.1152/ajpheart.91493.2007.PubMedCrossRef Singh, V. P., Baker, K. M., & Kumar, R. (2008). Activation of the intracellular renin–angiotensin system in cardiac fibroblasts by high glucose: Role in extracellular matrix production. American Journal of Physiology. Heart and Circulatory Physiology, 294(4), H1675–H1684. doi:10.​1152/​ajpheart.​91493.​2007.PubMedCrossRef
13.
Zurück zum Zitat Kim, N. N., Villarreal, F. J., Printz, M. P., Lee, A. A., & Dillmann, W. H. (1995). Trophic effects of angiotensin II on neonatal rat cardiac myocytes are mediated by cardiac fibroblasts. American Journal of Physiology, 269(3 Pt 1), E426–E437.PubMed Kim, N. N., Villarreal, F. J., Printz, M. P., Lee, A. A., & Dillmann, W. H. (1995). Trophic effects of angiotensin II on neonatal rat cardiac myocytes are mediated by cardiac fibroblasts. American Journal of Physiology, 269(3 Pt 1), E426–E437.PubMed
15.
Zurück zum Zitat Vlassara, H., & Palace, M. R. (2002). Diabetes and advanced glycation endproducts. Journal of Internal Medicine, 251(2), 87–101.PubMedCrossRef Vlassara, H., & Palace, M. R. (2002). Diabetes and advanced glycation endproducts. Journal of Internal Medicine, 251(2), 87–101.PubMedCrossRef
16.
Zurück zum Zitat Asbun, J., Manso, A. M., & Villarreal, F. J. (2005). Profibrotic influence of high glucose concentration on cardiac fibroblast functions: Effects of losartan and vitamin E. American Journal of Physiology. Heart and Circulatory Physiology, 288(1), H227–H234. doi:10.1152/ajpheart.00340.2004.PubMedCrossRef Asbun, J., Manso, A. M., & Villarreal, F. J. (2005). Profibrotic influence of high glucose concentration on cardiac fibroblast functions: Effects of losartan and vitamin E. American Journal of Physiology. Heart and Circulatory Physiology, 288(1), H227–H234. doi:10.​1152/​ajpheart.​00340.​2004.PubMedCrossRef
19.
21.
Zurück zum Zitat Stern, D. M., Yan, S. D., Yan, S. F., & Schmidt, A. M. (2002). Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes. Ageing Research Reviews, 1(1), 1–15.PubMedCrossRef Stern, D. M., Yan, S. D., Yan, S. F., & Schmidt, A. M. (2002). Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes. Ageing Research Reviews, 1(1), 1–15.PubMedCrossRef
22.
Zurück zum Zitat Bierhaus, A., Humpert, P. M., Morcos, M., Wendt, T., Chavakis, T., Arnold, B., Stern, D. M., & Nawroth, P. P. (2005). Understanding RAGE, the receptor for advanced glycation end products. Journal of Molecular Medicine (Berlin), 83(11), 876–886. doi:10.1007/s00109-005-0688-7.CrossRef Bierhaus, A., Humpert, P. M., Morcos, M., Wendt, T., Chavakis, T., Arnold, B., Stern, D. M., & Nawroth, P. P. (2005). Understanding RAGE, the receptor for advanced glycation end products. Journal of Molecular Medicine (Berlin), 83(11), 876–886. doi:10.​1007/​s00109-005-0688-7.CrossRef
23.
24.
Zurück zum Zitat Huang, J. S., Guh, J. Y., Hung, W. C., Yang, M. L., Lai, Y. H., Chen, H. C., & Chuang, L. Y. (1999). Role of the Janus kinase (JAK)/signal transducters and activators of transcription (STAT) cascade in advanced glycation end-product-induced cellular mitogenesis in NRK-49F cells. The Biochemical Journal, 342(Pt 1), 231–238.PubMedCrossRef Huang, J. S., Guh, J. Y., Hung, W. C., Yang, M. L., Lai, Y. H., Chen, H. C., & Chuang, L. Y. (1999). Role of the Janus kinase (JAK)/signal transducters and activators of transcription (STAT) cascade in advanced glycation end-product-induced cellular mitogenesis in NRK-49F cells. The Biochemical Journal, 342(Pt 1), 231–238.PubMedCrossRef
26.
Zurück zum Zitat Liu, X., Ostrom, R. S., & Insel, P. A. (2004). cAMP-elevating agents and adenylyl cyclase overexpression promote an antifibrotic phenotype in pulmonary fibroblasts. American Journal of Physiology. Cell Physiology, 286(5), C1089–C1099. doi:10.1152/ajpcell.00461.2003.PubMedCrossRef Liu, X., Ostrom, R. S., & Insel, P. A. (2004). cAMP-elevating agents and adenylyl cyclase overexpression promote an antifibrotic phenotype in pulmonary fibroblasts. American Journal of Physiology. Cell Physiology, 286(5), C1089–C1099. doi:10.​1152/​ajpcell.​00461.​2003.PubMedCrossRef
28.
Zurück zum Zitat Roberts, A. B., Sporn, M. B., Assoian, R. K., Smith, J. M., Roche, N. S., Wakefield, L. M., Heine, U. I., Liotta, L. A., Falanga, V., Kehrl, J. H., et al. (1986). Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro. Proceedings of the National Academy of Sciences of the United States of America, 83(12), 4167–4171.PubMedCrossRef Roberts, A. B., Sporn, M. B., Assoian, R. K., Smith, J. M., Roche, N. S., Wakefield, L. M., Heine, U. I., Liotta, L. A., Falanga, V., Kehrl, J. H., et al. (1986). Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro. Proceedings of the National Academy of Sciences of the United States of America, 83(12), 4167–4171.PubMedCrossRef
29.
Zurück zum Zitat Iwata, M., Cowling, R. T., Gurantz, D., Moore, C., Zhang, S., Yuan, J. X., & Greenberg, B. H. (2005). Angiotensin-(1–7) binds to specific receptors on cardiac fibroblasts to initiate antifibrotic and antitrophic effects. American Journal of Physiology. Heart and Circulatory Physiology, 289(6), H2356–H2363. doi:10.1152/ajpheart.00317.2005.PubMedCrossRef Iwata, M., Cowling, R. T., Gurantz, D., Moore, C., Zhang, S., Yuan, J. X., & Greenberg, B. H. (2005). Angiotensin-(1–7) binds to specific receptors on cardiac fibroblasts to initiate antifibrotic and antitrophic effects. American Journal of Physiology. Heart and Circulatory Physiology, 289(6), H2356–H2363. doi:10.​1152/​ajpheart.​00317.​2005.PubMedCrossRef
30.
Zurück zum Zitat Zahradka, P., Werner, J. P., Buhay, S., Litchie, B., Helwer, G., & Thomas, S. (2002). NF-kappaB activation is essential for angiotensin II-dependent proliferation and migration of vascular smooth muscle cells. Journal of Molecular and Cellular Cardiology, 34(12), 1609–1621.PubMedCrossRef Zahradka, P., Werner, J. P., Buhay, S., Litchie, B., Helwer, G., & Thomas, S. (2002). NF-kappaB activation is essential for angiotensin II-dependent proliferation and migration of vascular smooth muscle cells. Journal of Molecular and Cellular Cardiology, 34(12), 1609–1621.PubMedCrossRef
31.
Zurück zum Zitat Meszaros, J. G., Gonzalez, A. M., Endo-Mochizuki, Y., Villegas, S., Villarreal, F., & Brunton, L. L. (2000). Identification of G protein-coupled signaling pathways in cardiac fibroblasts: Cross talk between G(q) and G(s). American Journal of Physiology. Cell Physiology, 278(1), C154–C162.PubMed Meszaros, J. G., Gonzalez, A. M., Endo-Mochizuki, Y., Villegas, S., Villarreal, F., & Brunton, L. L. (2000). Identification of G protein-coupled signaling pathways in cardiac fibroblasts: Cross talk between G(q) and G(s). American Journal of Physiology. Cell Physiology, 278(1), C154–C162.PubMed
33.
Zurück zum Zitat Olivares-Reyes, J. A., Shah, B. H., Hernandez-Aranda, J., Garcia-Caballero, A., Farshori, M. P., Garcia-Sainz, J. A., & Catt, K. J. (2005). Agonist-induced interactions between angiotensin AT1 and epidermal growth factor receptors. Molecular Pharmacology, 68(2), 356–364. doi:10.1124/mol.104.010637.PubMed Olivares-Reyes, J. A., Shah, B. H., Hernandez-Aranda, J., Garcia-Caballero, A., Farshori, M. P., Garcia-Sainz, J. A., & Catt, K. J. (2005). Agonist-induced interactions between angiotensin AT1 and epidermal growth factor receptors. Molecular Pharmacology, 68(2), 356–364. doi:10.​1124/​mol.​104.​010637.PubMed
34.
Zurück zum Zitat Kamioka, M., Ishibashi, T., Sugimoto, K., Uekita, H., Nagai, R., Sakamoto N, et al. Blockade of renin–angiotensin system attenuates advanced glycation end products-mediated signaling pathways. Journal of Atherosclerosis and Thrombosis, 17(6), 590–600. Kamioka, M., Ishibashi, T., Sugimoto, K., Uekita, H., Nagai, R., Sakamoto N, et al. Blockade of renin–angiotensin system attenuates advanced glycation end products-mediated signaling pathways. Journal of Atherosclerosis and Thrombosis, 17(6), 590–600.
35.
Zurück zum Zitat Hattori, Y., Suzuki, M., Hattori, S., & Kasai, K. (2002). Vascular smooth muscle cell activation by glycated albumin (Amadori adducts). Hypertension, 39(1), 22–28.PubMedCrossRef Hattori, Y., Suzuki, M., Hattori, S., & Kasai, K. (2002). Vascular smooth muscle cell activation by glycated albumin (Amadori adducts). Hypertension, 39(1), 22–28.PubMedCrossRef
36.
Zurück zum Zitat Forbes, J. M., Thorpe, S. R., Thallas-Bonke, V., Pete, J., Thomas, M. C., Deemer, E. R., Bassal, S., El-Osta, A., Long, D. M., Panagiotopoulos, S., Jerums, G., Osicka, T. M., & Cooper, M. E. (2005). Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy. Journal of the American Society of Nephrology, 16(8), 2363–2372. doi:10.1681/ASN.2005010062.PubMedCrossRef Forbes, J. M., Thorpe, S. R., Thallas-Bonke, V., Pete, J., Thomas, M. C., Deemer, E. R., Bassal, S., El-Osta, A., Long, D. M., Panagiotopoulos, S., Jerums, G., Osicka, T. M., & Cooper, M. E. (2005). Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy. Journal of the American Society of Nephrology, 16(8), 2363–2372. doi:10.​1681/​ASN.​2005010062.PubMedCrossRef
37.
Zurück zum Zitat Nakamura, K., Yamagishi, S., Nakamura, Y., Takenaka, K., Matsui, T., Jinnouchi, Y., & Imaizumi, T. (2005). Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension. Microvascular Research, 70(3), 137–141. doi:10.1016/j.mvr.2005.10.002.PubMedCrossRef Nakamura, K., Yamagishi, S., Nakamura, Y., Takenaka, K., Matsui, T., Jinnouchi, Y., & Imaizumi, T. (2005). Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension. Microvascular Research, 70(3), 137–141. doi:10.​1016/​j.​mvr.​2005.​10.​002.PubMedCrossRef
38.
Zurück zum Zitat Tang, M., Zhong, M., Shang, Y., Lin, H., Deng, J., Jiang, H., Lu, H., Zhang, Y., & Zhang, W. (2008). Differential regulation of collagen types I and III expression in cardiac fibroblasts by AGEs through TRB3/MAPK signaling pathway. Cellular and Molecular Life Sciences, 65(18), 2924–2932. doi:10.1007/s00018-008-8255-3.PubMedCrossRef Tang, M., Zhong, M., Shang, Y., Lin, H., Deng, J., Jiang, H., Lu, H., Zhang, Y., & Zhang, W. (2008). Differential regulation of collagen types I and III expression in cardiac fibroblasts by AGEs through TRB3/MAPK signaling pathway. Cellular and Molecular Life Sciences, 65(18), 2924–2932. doi:10.​1007/​s00018-008-8255-3.PubMedCrossRef
39.
Zurück zum Zitat Huang, J. S., Guh, J. Y., Chen, H. C., Hung, W. C., Lai, Y. H., & Chuang, L. Y. (2001). Role of receptor for advanced glycation end-product (RAGE) and the JAK/STAT-signaling pathway in AGE-induced collagen production in NRK-49F cells. Journal of Cellular Biochemistry, 81(1), 102–113. doi:10.1002/1097-4644(20010401)81:1<102::AID-JCB1027>3.0.CO;2-Y.PubMedCrossRef Huang, J. S., Guh, J. Y., Chen, H. C., Hung, W. C., Lai, Y. H., & Chuang, L. Y. (2001). Role of receptor for advanced glycation end-product (RAGE) and the JAK/STAT-signaling pathway in AGE-induced collagen production in NRK-49F cells. Journal of Cellular Biochemistry, 81(1), 102–113. doi:10.1002/1097-4644(20010401)81:1<102::AID-JCB1027>3.0.CO;2-Y.PubMedCrossRef
40.
Zurück zum Zitat Forbes, J. M., Thomas, M. C., Thorpe, S. R., Alderson, N. L., & Cooper, M. E. (2004). The effects of valsartan on the accumulation of circulating and renal advanced glycation end products in experimental diabetes. Kidney International. Supplement, 92, S105–S107. doi:10.1111/j.1523-1755.2004.09225.x.PubMedCrossRef Forbes, J. M., Thomas, M. C., Thorpe, S. R., Alderson, N. L., & Cooper, M. E. (2004). The effects of valsartan on the accumulation of circulating and renal advanced glycation end products in experimental diabetes. Kidney International. Supplement, 92, S105–S107. doi:10.​1111/​j.​1523-1755.​2004.​09225.​x.PubMedCrossRef
41.
Zurück zum Zitat Ban, C. R., & Twigg, S. M. (2008). Fibrosis in diabetes complications: Pathogenic mechanisms and circulating and urinary markers. Vascular Health and Risk Management, 4(3), 575–596.PubMed Ban, C. R., & Twigg, S. M. (2008). Fibrosis in diabetes complications: Pathogenic mechanisms and circulating and urinary markers. Vascular Health and Risk Management, 4(3), 575–596.PubMed
42.
Zurück zum Zitat Daoud, S., Schinzel, R., Neumann, A., Loske, C., Fraccarollo, D., Diez, C., & Simm, A. (2001). Advanced glycation endproducts: Activators of cardiac remodeling in primary fibroblasts from adult rat hearts. Molecular Medicine, 7(8), 543–551.PubMed Daoud, S., Schinzel, R., Neumann, A., Loske, C., Fraccarollo, D., Diez, C., & Simm, A. (2001). Advanced glycation endproducts: Activators of cardiac remodeling in primary fibroblasts from adult rat hearts. Molecular Medicine, 7(8), 543–551.PubMed
43.
Zurück zum Zitat Henry, R. M., Paulus, W. J., Kamp, O., Kostense, P. J., Spijkerman, A. M., Dekker, J. M., Nijpels, G., Heine, R. J., Bouter, L. M., & Stehouwer, C. D. (2008). Deteriorating glucose tolerance status is associated with left ventricular dysfunction—the Hoorn Study. The Netherlands Journal of Medicine, 66(3), 110–117.PubMed Henry, R. M., Paulus, W. J., Kamp, O., Kostense, P. J., Spijkerman, A. M., Dekker, J. M., Nijpels, G., Heine, R. J., Bouter, L. M., & Stehouwer, C. D. (2008). Deteriorating glucose tolerance status is associated with left ventricular dysfunction—the Hoorn Study. The Netherlands Journal of Medicine, 66(3), 110–117.PubMed
44.
Zurück zum Zitat Mizushige, K., Yao, L., Noma, T., Kiyomoto, H., Yu, Y., Hosomi, N., Ohmori, K., & Matsuo, H. (2000). Alteration in left ventricular diastolic filling and accumulation of myocardial collagen at insulin-resistant prediabetic stage of a type II diabetic rat model. Circulation, 101(8), 899–907.PubMedCrossRef Mizushige, K., Yao, L., Noma, T., Kiyomoto, H., Yu, Y., Hosomi, N., Ohmori, K., & Matsuo, H. (2000). Alteration in left ventricular diastolic filling and accumulation of myocardial collagen at insulin-resistant prediabetic stage of a type II diabetic rat model. Circulation, 101(8), 899–907.PubMedCrossRef
45.
Zurück zum Zitat Reddy, V. S., Harskamp, R. E., van Ginkel, M. W., Calhoon, J., Baisden, C. E., Kim, I. S., Valente, A. J., & Chandrasekar, B. (2008). Interleukin-18 stimulates fibronectin expression in primary human cardiac fibroblasts via PI3K-Akt-dependent NF-kappaB activation. Journal of Cellular Physiology, 215(3), 697–707. doi:10.1002/jcp.21348.PubMedCrossRef Reddy, V. S., Harskamp, R. E., van Ginkel, M. W., Calhoon, J., Baisden, C. E., Kim, I. S., Valente, A. J., & Chandrasekar, B. (2008). Interleukin-18 stimulates fibronectin expression in primary human cardiac fibroblasts via PI3K-Akt-dependent NF-kappaB activation. Journal of Cellular Physiology, 215(3), 697–707. doi:10.​1002/​jcp.​21348.PubMedCrossRef
47.
Zurück zum Zitat Lee, C. I., Guh, J. Y., Chen, H. C., Hung, W. C., Yang, Y. L., & Chuang, L. Y. (2005). Advanced glycation end-product-induced mitogenesis and collagen production are dependent on angiotensin II and connective tissue growth factor in NRK-49F cells. Journal of Cellular Biochemistry, 95(2), 281–292. doi:10.1002/jcb.20380.PubMedCrossRef Lee, C. I., Guh, J. Y., Chen, H. C., Hung, W. C., Yang, Y. L., & Chuang, L. Y. (2005). Advanced glycation end-product-induced mitogenesis and collagen production are dependent on angiotensin II and connective tissue growth factor in NRK-49F cells. Journal of Cellular Biochemistry, 95(2), 281–292. doi:10.​1002/​jcb.​20380.PubMedCrossRef
48.
Zurück zum Zitat Bierhaus, A., Chevion, S., Chevion, M., Hofmann, M., Quehenberger, P., Illmer, T., Luther, T., Berentshtein, E., Tritschler, H., Muller, M., Wahl, P., Ziegler, R., & Nawroth, P. P. (1997). Advanced glycation end product-induced activation of NF-kappaB is suppressed by alpha-lipoic acid in cultured endothelial cells. Diabetes, 46(9), 1481–1490.PubMedCrossRef Bierhaus, A., Chevion, S., Chevion, M., Hofmann, M., Quehenberger, P., Illmer, T., Luther, T., Berentshtein, E., Tritschler, H., Muller, M., Wahl, P., Ziegler, R., & Nawroth, P. P. (1997). Advanced glycation end product-induced activation of NF-kappaB is suppressed by alpha-lipoic acid in cultured endothelial cells. Diabetes, 46(9), 1481–1490.PubMedCrossRef
Metadaten
Titel
Crosstalk Between the Renin–Angiotensin System and the Advance Glycation End Product Axis in the Heart: Role of the Cardiac Fibroblast
verfasst von
Katrina Go Yamazaki
Eileen Gonzalez
Alexander C. Zambon
Publikationsdatum
01.12.2012
Verlag
Springer US
Erschienen in
Journal of Cardiovascular Translational Research / Ausgabe 6/2012
Print ISSN: 1937-5387
Elektronische ISSN: 1937-5395
DOI
https://doi.org/10.1007/s12265-012-9405-4

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