nach oben

Erschienen in:

01.03.2020 | Original Contribution

M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment

verfasst von: Shaojun Liu, Jing Chen, Jian Shi, Wenyi Zhou, Li Wang, Weilun Fang, Yun Zhong, Xiaohui Chen, Yanfang Chen, Abdelkarim Sabri, Shiming Liu

Erschienen in: Basic Research in Cardiology | Ausgabe 2/2020

Einloggen, um Zugang zu erhalten

Abstract

The roles and the underlying mechanisms of M1-type macrophages in angiogenesis and postmyocardial infarction (MI) cardiac repair have remained unclear. In this study, we investigated the role of M1-like macrophage-derived exosomes in a MI microenvironment. We found that the proinflammatory M1-like-type macrophages released an extensive array of proinflammatory exosomes (M1-Exos) after MI. M1-Exos exerted an anti-angiogenic effect and accelerated MI injury. They also exhibited highly expressed proinflammatory miRNAs, such as miR-155. miR-155 was transferred to endothelial cells (ECs), leading to the inhibition of angiogenesis and cardiac dysfunction by downregulating its novel target genes, including Rac family small GTPase 1 (RAC1), p21 (RAC1)-activated kinase 2 (PAK2), Sirtuin 1 (Sirt1), and protein kinase AMP-activated catalytic subunit alpha 2 (AMPKα2). M1-Exos depressed Sirt1/AMPKα2–endothelial nitric oxide synthase and RAC1–PAK2 signaling pathways by simultaneously targeting the five molecule nodes (genes), reduced the angiogenic ability of ECs, aggravated myocardial injury, and restrained cardiac healing. The elucidation of this mechanism provides novel insights into the functional significance of M1 macrophages and their derived exosomes on angiogenesis and cardiac repair. This mechanism can be used as a novel potential therapeutic approach for the prevention and treatment of MI.

Nur mit Berechtigung zugänglich

Aurora AB, Porrello ER, Tan W, Mahmoud AI, Hill JA, Bassel-Duby R, Sadek HA, Olson EN (2014) Macrophages are required for neonatal heart regeneration. J Clin Invest 124:1382–1392. https://doi.org/10.1172/JCI72181 CrossRefPubMedPubMedCentral

Ben-Mordechai T, Holbova R, Landa-Rouben N, Harel-Adar T, Feinberg MS, Abd Elrahman I, Blum G, Epstein FH, Silman Z, Cohen S, Leor J (2013) Macrophage subpopulations are essential for infarct repair with and without stem cell therapy. J Am Coll Cardiol 62:1890–1901. https://doi.org/10.1016/j.jacc.2013.07.057 CrossRefPubMed

Ben-Mordechai T, Palevski D, Glucksam-Galnoy Y, Elron-Gross I, Margalit R, Leor J (2015) Targeting macrophage subsets for infarct repair. J Cardiovasc Pharmacol Ther 20:36–51. https://doi.org/10.1177/1074248414534916 CrossRefPubMed

Botker HE, Hausenloy D, Andreadou I, Antonucci S, Boengler K, Davidson SM, Deshwal S, Devaux Y, Di Lisa F, Di Sante M, Efentakis P, Femmino S, Garcia-Dorado D, Giricz Z, Ibanez B, Iliodromitis E, Kaludercic N, Kleinbongard P, Neuhauser M, Ovize M, Pagliaro P, Rahbek-Schmidt M, Ruiz-Meana M, Schluter KD, Schulz R, Skyschally A, Wilder C, Yellon DM, Ferdinandy P, Heusch G (2018) Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection. Basic Res Cardiol 113:39. https://doi.org/10.1007/s00395-018-0696-8 CrossRefPubMedPubMedCentral

Cheng Y, Rong J (2018) Macrophage polarization as a therapeutic target in myocardial infarction. Curr Drug Targets 19:651–662. https://doi.org/10.2174/1389450118666171031115025 CrossRefPubMed

Corliss BA, Azimi MS, Munson JM, Peirce SM, Murfee WL (2016) Macrophages: an inflammatory link between angiogenesis and lymphangiogenesis. Microcirculation 23:95–121. https://doi.org/10.1111/micc.12259 CrossRefPubMedPubMedCentral

Deveza L, Choi J, Yang F (2012) Therapeutic angiogenesis for treating cardiovascular diseases. Theranostics 2:801–814. https://doi.org/10.7150/thno.4419 CrossRefPubMedPubMedCentral

Eisenhardt SU, Weiss JB, Smolka C, Maxeiner J, Pankratz F, Bemtgen X, Kustermann M, Thiele JR, Schmidt Y, Bjoern Stark G, Moser M, Bode C, Grundmann S (2015) MicroRNA-155 aggravates ischemia-reperfusion injury by modulation of inflammatory cell recruitment and the respiratory oxidative burst. Basic Res Cardiol 110:32. https://doi.org/10.1007/s00395-015-0490-9 CrossRefPubMed

Frangogiannis NG (2015) Inflammation in cardiac injury, repair and regeneration. Curr Opin Cardiol 30:240–245. https://doi.org/10.1097/HCO.0000000000000158 CrossRefPubMedPubMedCentral

10.

Guo J, Liu HB, Sun C, Yan XQ, Hu J, Yu J, Yuan Y, Du ZM (2019) MicroRNA-155 promotes myocardial infarction-induced apoptosis by targeting RNA-binding protein QKI. Oxid Med Cell Longev 2019:4579806. https://doi.org/10.1155/2019/4579806 CrossRefPubMedPubMedCentral

11.

Harel-Adar T, Ben Mordechai T, Amsalem Y, Feinberg MS, Leor J, Cohen S (2011) Modulation of cardiac macrophages by phosphatidylserine-presenting liposomes improves infarct repair. Proc Natl Acad Sci USA 108:1827–1832. https://doi.org/10.1073/pnas.1015623108 CrossRefPubMed

12.

Hausenloy DJ, Chilian W, Crea F, Davidson SM, Ferdinandy P, Garcia-Dorado D, van Royen N, Schulz R, Heusch G (2019) The coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection. Cardiovasc Res 115:1143–1155. https://doi.org/10.1093/cvr/cvy286 CrossRefPubMed

13.

He W, Huang H, Xie Q, Wang Z, Fan Y, Kong B, Huang D, Xiao Y (2016) MiR-155 knockout in fibroblasts improves cardiac remodeling by targeting tumor protein p53-inducible nuclear protein 1. J Cardiovasc Pharmacol Ther 21:423–435. https://doi.org/10.1177/1074248415616188 CrossRefPubMed

14.

Hesketh M, Sahin KB, West ZE, Murray RZ (2017) Macrophage phenotypes regulate scar formation and chronic wound healing. Int J Mol Sci. https://doi.org/10.3390/ijms18071545 CrossRefPubMedPubMedCentral

15.

Heusch G (2016) The coronary circulation as a target of cardioprotection. Circ Res 118:1643–1658. https://doi.org/10.1161/CIRCRESAHA.116.308640 CrossRefPubMed

16.

Heusch G (2019) Coronary microvascular obstruction: the new frontier in cardioprotection. Basic Res Cardiol 114:45. https://doi.org/10.1007/s00395-019-0756-8 CrossRefPubMed

17.

Hu J, Huang CX, Rao PP, Cao GQ, Zhang Y, Zhou JP, Zhu LY, Liu MX, Zhang GG (2019) MicroRNA-155 inhibition attenuates endoplasmic reticulum stress-induced cardiomyocyte apoptosis following myocardial infarction via reducing macrophage inflammation. Eur J Pharmacol 857:172449. https://doi.org/10.1016/j.ejphar.2019.172449 CrossRefPubMed

18.

Hu J, Huang CX, Rao PP, Zhou JP, Wang X, Tang L, Liu MX, Zhang GG (2019) Inhibition of microRNA-155 attenuates sympathetic neural remodeling following myocardial infarction via reducing M1 macrophage polarization and inflammatory responses in mice. Eur J Pharmacol 851:122–132. https://doi.org/10.1016/j.ejphar.2019.02.001 CrossRefPubMed

19.

Hu M, Guo G, Huang Q, Cheng C, Xu R, Li A, Liu N, Liu S (2018) The harsh microenvironment in infarcted heart accelerates transplanted bone marrow mesenchymal stem cells injury: the role of injured cardiomyocytes-derived exosomes. Cell Death Dis 9:357. https://doi.org/10.1038/s41419-018-0392-5 CrossRefPubMedPubMedCentral

20.

Hu Y, Zhang H, Lu Y, Bai H, Xu Y, Zhu X, Zhou R, Ben J, Xu Y, Chen Q (2011) Class A scavenger receptor attenuates myocardial infarction-induced cardiomyocyte necrosis through suppressing M1 macrophage subset polarization. Basic Res Cardiol 106:1311–1328. https://doi.org/10.1007/s00395-011-0204-x CrossRefPubMed

21.

Ishikawa S, Noma T, Fu HY, Matsuzaki T, Ishizawa M, Ishikawa K, Murakami K, Nishimoto N, Nishiyama A, Minamino T (2017) Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice. PLoS ONE 12:e0187894. https://doi.org/10.1371/journal.pone.0187894 CrossRefPubMedPubMedCentral

22.

Jablonski KA, Gaudet AD, Amici SA, Popovich PG, Guerau-de-Arellano M (2016) Control of the inflammatory macrophage transcriptional signature by miR-155. PLoS ONE 11:e0159724. https://doi.org/10.1371/journal.pone.0159724 CrossRefPubMedPubMedCentral

23.

Jeppesen DK, Fenix AM, Franklin JL, Higginbotham JN, Zhang Q, Zimmerman LJ, Liebler DC, Ping J, Liu Q, Evans R, Fissell WH, Patton JG, Rome LH, Burnette DT, Coffey RJ (2019) Reassessment of exosome composition. Cell 177(428–445):e418. https://doi.org/10.1016/j.cell.2019.02.029 CrossRef

24.

Jetten N, Verbruggen S, Gijbels MJ, Post MJ, De Winther MP, Donners MM (2014) Anti-inflammatory M2, but not pro-inflammatory M1 macrophages promote angiogenesis in vivo. Angiogenesis 17:109–118. https://doi.org/10.1007/s10456-013-9381-6 CrossRefPubMed

25.

Jung M, Dodsworth M, Thum T (2018) Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction. Basic Res Cardiol 114:4. https://doi.org/10.1007/s00395-018-0712-z CrossRefPubMedPubMedCentral

26.

Koh W, Mahan RD, Davis GE (2008) Cdc42- and Rac1-mediated endothelial lumen formation requires Pak2, Pak4 and Par3, and PKC-dependent signaling. J Cell Sci 121:989–1001. https://doi.org/10.1242/jcs.020693 CrossRefPubMed

27.

Kong W, He L, Richards EJ, Challa S, Xu CX, Permuth-Wey J, Lancaster JM, Coppola D, Sellers TA, Djeu JY, Cheng JQ (2014) Upregulation of miRNA-155 promotes tumour angiogenesis by targeting VHL and is associated with poor prognosis and triple-negative breast cancer. Oncogene 33:679–689. https://doi.org/10.1038/onc.2012.636 CrossRefPubMed

28.

Kroller-Schon S, Jansen T, Tran TLP, Kvandova M, Kalinovic S, Oelze M, Keaney JF Jr, Foretz M, Viollet B, Daiber A, Kossmann S, Lagrange J, Frenis K, Wenzel P, Munzel T, Schulz E (2019) Endothelial alpha1AMPK modulates angiotensin II-mediated vascular inflammation and dysfunction. Basic Res Cardiol 114:8. https://doi.org/10.1007/s00395-019-0717-2 CrossRefPubMed

29.

Lambert JM, Lopez EF, Lindsey ML (2008) Macrophage roles following myocardial infarction. Int J Cardiol 130:147–158. https://doi.org/10.1016/j.ijcard.2008.04.059 CrossRefPubMedPubMedCentral

30.

Lan J, Sun L, Xu F, Liu L, Hu F, Song D, Hou Z, Wu W, Luo X, Wang J, Yuan X, Hu J, Wang G (2019) M2 macrophage-derived exosomes promote cell migration and invasion in colon cancer. Cancer Res 79:146–158. https://doi.org/10.1158/0008-5472.CAN-18-0014 CrossRefPubMed

31.

Lawrence T, Natoli G (2011) Transcriptional regulation of macrophage polarization: enabling diversity with identity. Nat Rev Immunol 11:750–761. https://doi.org/10.1038/nri3088 CrossRefPubMed

32.

Lee HD, Kim YH, Kim DS (2014) Exosomes derived from human macrophages suppress endothelial cell migration by controlling integrin trafficking. Eur J Immunol 44:1156–1169. https://doi.org/10.1002/eji.201343660 CrossRefPubMed

33.

Leuschner F, Dutta P, Gorbatov R, Novobrantseva TI, Donahoe JS, Courties G, Lee KM, Kim JI, Markmann JF, Marinelli B, Panizzi P, Lee WW, Iwamoto Y, Milstein S, Epstein-Barash H, Cantley W, Wong J, Cortez-Retamozo V, Newton A, Love K, Libby P, Pittet MJ, Swirski FK, Koteliansky V, Langer R, Weissleder R, Anderson DG, Nahrendorf M (2011) Therapeutic siRNA silencing in inflammatory monocytes in mice. Nat Biotechnol 29:1005–1010. https://doi.org/10.1038/nbt.1989 CrossRefPubMedPubMedCentral

34.

Li J, Li SH, Wu J, Weisel RD, Yao A, Stanford WL, Liu SM, Li RK (2018) Young bone marrow Sca-1 cells rejuvenate the aged heart by promoting epithelial-to-mesenchymal transition. Theranostics 8:1766–1781. https://doi.org/10.7150/thno.22788 CrossRefPubMedPubMedCentral

35.

Lindsey ML, Bolli R, Canty JM Jr, Du XJ, Frangogiannis NG, Frantz S, Gourdie RG, Holmes JW, Jones SP, Kloner RA, Lefer DJ, Liao R, Murphy E, Ping P, Przyklenk K, Recchia FA, Schwartz Longacre L, Ripplinger CM, Van Eyk JE, Heusch G (2018) Guidelines for experimental models of myocardial ischemia and infarction. Am J Physiol Heart Circ Physiol 314:H812–H838. https://doi.org/10.1152/ajpheart.00335.2017 CrossRefPubMedPubMedCentral

36.

Lindsey ML, Kassiri Z, Virag JAI, de Castro Bras LE, Scherrer-Crosbie M (2018) Guidelines for measuring cardiac physiology in mice. Am J Physiol Heart Circ Physiol 314:H733–H752. https://doi.org/10.1152/ajpheart.00339.2017 CrossRefPubMedPubMedCentral

37.

Lindsey ML, Saucerman JJ, DeLeon-Pennell KY (2016) Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction. Biochim Biophys Acta 1862:2288–2292. https://doi.org/10.1016/j.bbadis.2016.05.013 CrossRefPubMedPubMedCentral

38.

Liu T, Shen D, Xing S, Chen J, Yu Z, Wang J, Wu B, Chi H, Zhao H, Liang Z, Chen C (2013) Attenuation of exogenous angiotensin II stress-induced damage and apoptosis in human vascular endothelial cells via microRNA-155 expression. Int J Mol Med 31:188–196. https://doi.org/10.3892/ijmm.2012.1182 CrossRefPubMed

39.

Lu L, McCurdy S, Huang S, Zhu X, Peplowska K, Tiirikainen M, Boisvert WA, Garmire LX (2016) Time series miRNA-mRNA integrated analysis reveals critical miRNAs and targets in macrophage polarization. Sci Rep 6:37446. https://doi.org/10.1038/srep37446 CrossRefPubMedPubMedCentral

40.

Ma Y, Mouton AJ, Lindsey ML (2018) Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction. Transl Res 191:15–28. https://doi.org/10.1016/j.trsl.2017.10.001 CrossRefPubMed

41.

Marinkovic G, Heemskerk N, van Buul JD, de Waard V (2015) The ins and outs of small GTPase Rac1 in the vasculature. J Pharmacol Exp Ther 354:91–102. https://doi.org/10.1124/jpet.115.223610 CrossRefPubMed

42.

Martinez FO, Gordon S (2014) The M1 and M2 paradigm of macrophage activation: time for reassessment. F1000Prime Rep 6:13. https://doi.org/10.12703/P6-13 CrossRefPubMedPubMedCentral

43.

Mouton AJ, DeLeon-Pennell KY, Rivera Gonzalez OJ, Flynn ER, Freeman TC, Saucerman JJ, Garrett MR, Ma Y, Harmancey R, Lindsey ML (2018) Mapping macrophage polarization over the myocardial infarction time continuum. Basic Res Cardiol 113:26. https://doi.org/10.1007/s00395-018-0686-x CrossRefPubMedPubMedCentral

44.

Osada-Oka M, Shiota M, Izumi Y, Nishiyama M, Tanaka M, Yamaguchi T, Sakurai E, Miura K, Iwao H (2017) Macrophage-derived exosomes induce inflammatory factors in endothelial cells under hypertensive conditions. Hypertens Res 40:353–360. https://doi.org/10.1038/hr.2016.163 CrossRefPubMed

45.

Ostrowski M, Carmo NB, Krumeich S, Fanget I, Raposo G, Savina A, Moita CF, Schauer K, Hume AN, Freitas RP, Goud B, Benaroch P, Hacohen N, Fukuda M, Desnos C, Seabra MC, Darchen F, Amigorena S, Moita LF, Thery C (2010) Rab27a and Rab27b control different steps of the exosome secretion pathway. Nat Cell Biol 12:19–30. https://doi.org/10.1038/ncb2000(sup pp 11–13) CrossRefPubMed

46.

Panizzi P, Swirski FK, Figueiredo JL, Waterman P, Sosnovik DE, Aikawa E, Libby P, Pittet M, Weissleder R, Nahrendorf M (2010) Impaired infarct healing in atherosclerotic mice with Ly-6C(hi) monocytosis. J Am Coll Cardiol 55:1629–1638. https://doi.org/10.1016/j.jacc.2009.08.089 CrossRefPubMedPubMedCentral

47.

Pankratz F, Bemtgen X, Zeiser R, Leonhardt F, Kreuzaler S, Hilgendorf I, Smolka C, Helbing T, Hoefer I, Esser JS, Kustermann M, Moser M, Bode C, Grundmann S (2015) MicroRNA-155 exerts cell-specific antiangiogenic but proarteriogenic effects during adaptive neovascularization. Circulation 131:1575–1589. https://doi.org/10.1161/CIRCULATIONAHA.114.014579 CrossRefPubMed

48.

Podaru MN, Fields L, Kainuma S, Ichihara Y, Hussain M, Ito T, Kobayashi K, Mathur A, D'Acquisto F, Lewis-McDougall F, Suzuki K (2019) Reparative macrophage transplantation for myocardial repair: a refinement of bone marrow mononuclear cell-based therapy. Basic Res Cardiol 114:34. https://doi.org/10.1007/s00395-019-0742-1 CrossRefPubMedPubMedCentral

49.

Richards J, Gabunia K, Kelemen SE, Kako F, Choi ET, Autieri MV (2015) Interleukin-19 increases angiogenesis in ischemic hind limbs by direct effects on both endothelial cells and macrophage polarization. J Mol Cell Cardiol 79:21–31. https://doi.org/10.1016/j.yjmcc.2014.11.002 CrossRefPubMed

50.

Tang N, Sun B, Gupta A, Rempel H, Pulliam L (2016) Monocyte exosomes induce adhesion molecules and cytokines via activation of NF-kappaB in endothelial cells. FASEB J 30:3097–3106. https://doi.org/10.1096/fj.201600368RR CrossRefPubMedPubMedCentral

51.

ter Horst EN, Hakimzadeh N, van der Laan AM, Krijnen PA, Niessen HW, Piek JJ (2015) Modulators of macrophage polarization influence healing of the infarcted myocardium. Int J Mol Sci 16:29583–29591. https://doi.org/10.3390/ijms161226187 CrossRefPubMedPubMedCentral

52.

van der Vorst EPC, Weber C (2019) Novel features of monocytes and macrophages in cardiovascular biology and disease. Arterioscler Thromb Vasc Biol 39:e30–e37. https://doi.org/10.1161/ATVBAHA.118.312002 CrossRefPubMed

53.

Verderio C, Gabrielli M, Giussani P (2018) Role of sphingolipids in the biogenesis and biological activity of extracellular vesicles. J Lipid Res 59:1325–1340. https://doi.org/10.1194/jlr.R083915 CrossRefPubMedPubMedCentral

54.

Wang C, Zhang C, Liu L, Axx X, Chen B, Li Y, Du J (2017) Macrophage-derived mir-155-containing exosomes suppress fibroblast proliferation and promote fibroblast inflammation during cardiac injury. Mol Ther 25:192–204. https://doi.org/10.1016/j.ymthe.2016.09.001 CrossRefPubMedPubMedCentral

55.

Weber M, Kim S, Patterson N, Rooney K, Searles CD (2014) MiRNA-155 targets myosin light chain kinase and modulates actin cytoskeleton organization in endothelial cells. Am J Physiol Heart Circ Physiol 306:H1192–1203. https://doi.org/10.1152/ajpheart.00521.2013 CrossRefPubMedPubMedCentral

56.

Williams JW, Giannarelli C, Rahman A, Randolph GJ, Kovacic JC (2018) Macrophage biology, classification, and phenotype in cardiovascular disease: JACC macrophage in CVD series (Part 1). J Am Coll Cardiol 72:2166–2180. https://doi.org/10.1016/j.jacc.2018.08.2148 CrossRefPubMedPubMedCentral

57.

Wu R, Gao W, Yao K, Ge J (2019) Roles of exosomes derived from immune cells in cardiovascular diseases. Front Immunol 10:648. https://doi.org/10.3389/fimmu.2019.00648 CrossRefPubMedPubMedCentral

58.

Ying W, Riopel M, Bandyopadhyay G, Dong Y, Birmingham A, Seo JB, Ofrecio JM, Wollam J, Hernandez-Carretero A, Fu W, Li P, Olefsky JM (2017) Adipose tissue macrophage-derived exosomal mirnas can modulate in vivo and in vitro insulin sensitivity. Cell 171(372–384):e312. https://doi.org/10.1016/j.cell.2017.08.035 CrossRef

59.

Yuan A, Hsiao YJ, Chen HY, Chen HW, Ho CC, Chen YY, Liu YC, Hong TH, Yu SL, Chen JJ, Yang PC (2015) Opposite effects of M1 and M2 macrophage subtypes on lung cancer progression. Sci Rep 5:14273. https://doi.org/10.1038/srep14273 CrossRefPubMedPubMedCentral

60.

Zhang Y, Zhang M, Li X, Tang Z, Wang X, Zhong M, Suo Q, Zhang Y, Lv K (2016) Silencing microRNA-155 attenuates cardiac injury and dysfunction in viral myocarditis via promotion of M2 phenotype polarization of macrophages. Sci Rep 6:22613. https://doi.org/10.1038/srep22613 CrossRefPubMedPubMedCentral

61.

Zheng B, Yin WN, Suzuki T, Zhang XH, Zhang Y, Song LL, Jin LS, Zhan H, Zhang H, Li JS, Wen JK (2017) Exosome-mediated miR-155 transfer from smooth muscle cells to endothelial cells induces endothelial injury and promotes atherosclerosis. Mol Ther 25:1279–1294. https://doi.org/10.1016/j.ymthe.2017.03.031 CrossRefPubMedPubMedCentral

62.

Zheng P, Luo Q, Wang W, Li J, Wang T, Wang P, Chen L, Zhang P, Chen H, Liu Y, Dong P, Xie G, Ma Y, Jiang L, Yuan X, Shen L (2018) Tumor-associated macrophages-derived exosomes promote the migration of gastric cancer cells by transfer of functional apolipoprotein E. Cell Death Dis 9:434. https://doi.org/10.1038/s41419-018-0465-5 CrossRefPubMedPubMedCentral

63.

Zhou J, Bai W, Liu Q, Cui J, Zhang W (2018) Intermittent hypoxia enhances THP-1 monocyte adhesion and chemotaxis and promotes M1 macrophage polarization via RAGE. Biomed Res Int 2018:1650456. https://doi.org/10.1155/2018/1650456 CrossRefPubMedPubMedCentral

64.

Zhu N, Zhang D, Chen S, Liu X, Lin L, Huang X, Guo Z, Liu J, Wang Y, Yuan W, Qin Y (2011) Endothelial enriched microRNAs regulate angiotensin II-induced endothelial inflammation and migration. Atherosclerosis 215:286–293. https://doi.org/10.1016/j.atherosclerosis.2010.12.024 CrossRefPubMed

Titel: M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment
verfasst von: Shaojun Liu
Jing Chen
Jian Shi
Wenyi Zhou
Li Wang
Weilun Fang
Yun Zhong
Xiaohui Chen
Yanfang Chen
Abdelkarim Sabri
Shiming Liu
Publikationsdatum: 01.03.2020
Verlag: Springer Berlin Heidelberg
Erschienen in: Basic Research in Cardiology / Ausgabe 2/2020
Print ISSN: 0300-8428
Elektronische ISSN: 1435-1803
DOI: https://doi.org/10.1007/s00395-020-0781-7

Neu im Fachgebiet Kardiologie

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

17.05.2024 Plötzlicher Herztod Nachrichten

Ein signifikanter Anteil der Fälle von plötzlichem Herztod ist genetisch bedingt. Um ihre Verwandten vor diesem Schicksal zu bewahren, sollten jüngere Personen, die plötzlich unerwartet versterben, ausnahmslos einer Autopsie unterzogen werden.

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

17.05.2024 Direkte orale Antikoagulanzien Nachrichten

Kommt es zu einer nichttraumatischen Hirnblutung, spielt es keine große Rolle, ob die Betroffenen zuvor direkt wirksame orale Antikoagulanzien oder Marcumar bekommen haben: Die Prognose ist ähnlich schlecht.

Schlechtere Vorhofflimmern-Prognose bei kleinem linken Ventrikel

17.05.2024 Vorhofflimmern Nachrichten

Nicht nur ein vergrößerter, sondern auch ein kleiner linker Ventrikel ist bei Vorhofflimmern mit einer erhöhten Komplikationsrate assoziiert. Der Zusammenhang besteht nach Daten aus China unabhängig von anderen Risikofaktoren.

Semaglutid bei Herzinsuffizienz: Wie erklärt sich die Wirksamkeit?

17.05.2024 Herzinsuffizienz Nachrichten

Bei adipösen Patienten mit Herzinsuffizienz des HFpEF-Phänotyps ist Semaglutid von symptomatischem Nutzen. Resultiert dieser Benefit allein aus der Gewichtsreduktion oder auch aus spezifischen Effekten auf die Herzinsuffizienz-Pathogenese? Eine neue Analyse gibt Aufschluss.

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Die Highlights vom Kongress des American College of Cardiology 2024

Springer Medizin

M1-like macrophage-derived exosomes suppress angiogenesis and exacerbate cardiac dysfunction in a myocardial infarction microenvironment

Abstract

Neu im Fachgebiet Kardiologie

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

Schlechtere Vorhofflimmern-Prognose bei kleinem linken Ventrikel

Semaglutid bei Herzinsuffizienz: Wie erklärt sich die Wirksamkeit?

Update Kardiologie

Die Highlights vom Kongress des American College of Cardiology 2024

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 2/2020

Murine sca1/flk1-positive cells are not endothelial progenitor cells, but B2 lymphocytes

Perturbations in myocardial perfusion and oxygen balance in swine with multiple risk factors: a novel model of ischemia and no obstructive coronary artery disease

DNA-PKcs promotes cardiac ischemia reperfusion injury through mitigating BI-1-governed mitochondrial homeostasis

Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice

FHL-1 is not involved in pressure overload-induced maladaptive right ventricular remodeling and dysfunction

Thrombin receptor PAR4 drives canonical NLRP3 inflammasome signaling in the heart

Neu im Fachgebiet Kardiologie

„Jeder Fall von plötzlichem Tod muss obduziert werden!“

Hirnblutung unter DOAK und VKA ähnlich bedrohlich

Schlechtere Vorhofflimmern-Prognose bei kleinem linken Ventrikel

Semaglutid bei Herzinsuffizienz: Wie erklärt sich die Wirksamkeit?

Update Kardiologie