Advances in research on the role of T cell subsets in ventricular remodeling

doi:10.3969.j.issn.1671-7856.2017.10.017

Home > Archive>Volume 27, Issue 10, 2017 >85-88. DOI:10.3969.j.issn.1671-7856.2017.10.017

Advances in research on the role of T cell subsets in ventricular remodeling
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                        10.3969.j.issn.1671-7856.2017.10.017
                    
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                        GU Wen-chaoGU Wen-chao
Department of Cardiac Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
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ZHOU Xiao-huiZHOU Xiao-hui
Research Center for Translational Medicine, Tongji University School of Medicine, Shanghai 200120;Shanghai Heart Failure Institute, Shanghai 200120
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LIN FangLIN Fang
Research Center for Translational Medicine, Tongji University School of Medicine, Shanghai 200120;Shanghai Heart Failure Institute, Shanghai 200120
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FAN Hui-minFAN Hui-min
Department of Cardiac Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China;Research Center for Translational Medicine, Tongji University School of Medicine, Shanghai 200120;Shanghai Heart Failure Institute, Shanghai 200120
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Abstract:

Ventricular remodeling is one of the main causes of heart failure. A large number of studies have shown that inflammation plays an important role in the occurrence and development of ventricular remodeling. Recent studies found that chronic inflammation mediated by T cells is closely related to the progression of ventricular remodeling. This review summarized the recent research progress of T lymphocyte subsets in ventricular remodeling.

Key words:Inflammation;T lymphocytes;Ventricular remodeling

Reference

[1] 张辉,周晓慧,刘中民,等.生物学标志物在心力衰竭早期诊断中作用的研究进展[J].中国实验动物学报,2016,(01):102-106.

[2] Huber SA, Feldman AM, Sartini D. Coxsackievirus B3 induces T regulatory cells, which inhibit cardiomyopathy in tumor necrosis factor-alpha transgenic mice[J]. Circ Res,2006, 99(10):1109-1116.

[3] Laroumanie F, Douin-Echinard V, Pozzo J, et al. CD4⁺ T cells promote the transition from hypertrophy to heart failure during chronic pressure overload[J]. Circulation, 2014, 129(21):2111-2124.

[4] Guzik TJ, Hoch NE, Brown KA, et al. Role of the T cell in the genesis of angiotensin Ⅱ induced hypertension and vascular dysfunction[J]. J Exp Med, 2007, 204(10):2449-2460.

[5] Abdullah CS, Li Z, Wang X, et al. Depletion of T lymphocytes ameliorates cardiac fibrosis in streptozotocin-induced diabetic cardiomyopathy[J].Int Immunopharmacol, 2016, 39:251-264.

[6] Pasqui AL, Di Renzo M, Auteri A, et al. Cytokines in acute coronary syndromes[J]. Int J Cardiol, 2005, 105(3):355-356.

[7] Engelbertsen D, Andersson L, Ljungcrantz I, et al. T-helper 2 immunity is associated with reduced risk of myocardial infarction and stroke[J]. Arterioscler Thromb Vasc Biol, 2013, 33(3):637-644.

[8] Yan X, Anzai A, Katsumata Y, et al. Temporal dynamics of cardiac immune cell accumulation following acute myocardial infarction[J]. J Mol Cell Cardiol, 2013, 62:24-35.

[9] Tapp LD, Shantsila E, Wrigley BJ, et al. The CD14⁺⁺CD16⁺ monocyte subset and monocyte-platelet interactions in patients with ST-elevation myocardial infarction[J]. J Thromb Haemost, 2012, 10(7):1231-1241.

[10] Liao YH, Xia N, Zhou SF, et al. Interleukin-17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration[J]. J Am Coll Cardiol, 2012, 59(4):420-429.

[11] Liu W, Wang X, Feng W, et al. Lentivirus mediated IL-17R blockade improves diastolic cardiac function in spontaneously hypertensive rats[J]. Exp Mol Pathol, 2011, 91(1):362-367.

[12] Madhur MS, Lob HE, McCann LA, et al. Interleukin 17 promotes angiotensin Ⅱ-induced hypertension and vascular dysfunction[J]. Hypertension, 2010, 55(2):500-507.

[13] Baldeviano GC, Barin JG, Talor MV, et al. Interleukin-17A is dispensable for myocarditis but essential for the progression to dilated cardiomyopathy[J]. Circ Res, 2010, 106(10):1646-1655.

[14] Lin YZ, Wu BW, Lu ZD, et al. Circulating Th22 and Th9 levels in patients with acute coronary syndrome[J]. Mediators Inflamm, 2013, 2013:635672.

[15] Qing K, Weifeng W, Fan Y, et al. Distinct different expression of Th17 and Th9 cells in coxsackie virus B3-induced mice viral myocarditis[J]. Vi捲瑯楬漠湊?愠渲搰?挱愬渠?爺攲挶漷朮渼楢穲放?愱渶摝?歇楨汯汵?桢敡慮汩琠桇祡?浡祲漠捓礬琠敁獮?楡湬?癢椠瑁爬漠孈?嵳?????潍氬??整氠污??愠牃摄椴漼汳??资???????ㄠ??????????????扵牰?嬠??嵥??慡楮獤攠汩?????敏獓愼牳極潰￣????慵楰爾搠?卵??敥瑴?愠汩???硡灴敩牥楮浴敳渠瑷慩汴?愠畭瑹潯楣浡浲畤湩敡?洠祩潮捦慡牲摣楴瑩楯獮?灊牝漮搠畉捲敡摮?扊礠?慭摭潵灮瑯楬瘬攠′琰爱愲測猠昹攨爱?漺昵″猭瀶氰攮渼潢捲社瑛攱猷?愠晗瑩敧牲?浮礠潍挬愠牂摪楯慲汫?楡湣晫慡爠捈琬椠潁湮孤?嵲???楮爠捌?删敥獴????????㈠?????????????扣牵?孡??嵮?娠桃潄甴?塳??吾愫渼术???￣?慯潸????敵瑰￣愫氼??呵楰猾猠畔攠?牥敬獬楳搠敡湲瑥?牡敳杳畯汣慩瑡潴牥祤?呷?捴敨氠污獮?湩潮癣敲汥?瑳桥敤爠慲灩敳畫琠楦捯?琠慤牥杶敥瑬獯?晭潥牮?栠畯浦愠湭?摯楣獡敲慤獩敡孬?嵩???敲汣汴??潮氠??浴洠畮湯潴氠??????????????????????scler Thromb Vasc Biol, 2012, 32(8):2000-2004.

[18] Kanellakis P, Dinh TN, Agrotis A, et al. CD4⁺CD25⁺Foxp3⁺ regulatory T cells suppress cardiac fibrosis in the hypertensive heart[J]. J Hypertens, 2011, 29(9):1820-1828.

[19] Dobaczewski M, Xia Y, Bujak M, et al. CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells[J]. Am J Pathol, 2010, 176(5):2177-2187.

[20] Sharir R, Semo J, Shimoni S, et al. Experimental myocardial infarction induces altered regulatory T cell hemostasis, and adoptive transfer attenuates subsequent remodeling[J]. PLoS One, 2014, 9(12):e113653.

[21] Saxena A, Dobaczewski M, Rai V, et al. Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function[J]. Am J Physiol Heart Circ Physiol, 2014, 307(8):H1233-1242.

[22] Weirather J, Hofmann UD, Beyersdorf N, et al. CD4⁺Foxp3⁺ T cells improve healing after myocardial infarction by modulating monocyte/macrophage differentiation[J]. Circ Res, 2014, 115(1):55-67.

[23] Tang TT, Yuan J, Zhu ZF, et al. Regulatory T cells ameliorate cardiac remodeling after myocardial infarction[J]. Basic Res Cardiol, 2012, 107(1):232.

[24] Tae Yu H, Youn JC, Lee J, et al. Characterization of CD8⁺CD57⁺ T cells in patients with acute myocardial infarction[J]. Cell Mol Immunol, 2015;12(4):466-473.

[25] Varda-Bloom N, Leor J, Ohad DG, et al. Cytotoxic T lymphocytes are activated following myocardial infar

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Received:February 16,2017
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Online: October 23,2017
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