S100A4 protects the myocardium against ischemic stress.

S100A4 protects the myocardium against ischemic stress.
复制标题

DOI:
10.1016/j.yjmcc.2016.10.001
复制
发表时间:
2016-11
影响因子:
5
通讯作者:
Völkers M
Völkers M
中科院分区:
医学2区
文献类型:
--
作者:
Doroudgar S;Quijada P;Konstandin M;Ilves K;Broughton K;Khalafalla FG;Casillas A;Nguyen K;Gude N;Toko H;Ornelas L;Thuerauf DJ;Glembotski CC;Sussman MA;Völkers M

文献摘要

参考文献

被引文献

相似文献

Myocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue fibrosis. S100A4 protein plays multiple roles in cellular survival, and tissue fibrosis, but the relative role of the S100A4 in the myocardium after myocardial infarction is unknown. This study aims to investigate the role of S100A4 in myocardial remodeling and cardiac function following infarct damage. S100A4 expression is low in the adult myocardium, but significantly increased following myocardial infarction. Deletion of S100A4 increased cardiac damage after myocardial infarction, whereas cardiac myocyte-specific overexpression of S100A4 protected the infarcted myocardium. Decreased cardiac function in S100A4 Knockout mice was accompanied with increased cardiac remodeling, fibrosis, and diminished capillary density in the remote myocardium. Loss of S100A4 caused increased apoptotic cell death both in vitro and in vivo in part mediated by decreased VEGF expression. Conversely, S100A4 overexpression protected cells against apoptosis in vitro and in vivo. Increased pro-survival AKT-signaling explained reduced apoptosis in S100A4 overexpressing cells. S100A4 expression protects cardiac myocytes against myocardial ischemia and is required for stabilization of cardiac function after MI.
DOI: 10.1016/j.yjmcc.2008.04.011
发表时间: 2008-07-01
影响因子: 5
作者:
Lin, Heng-Huei;Chen, Yen-Hui;Chau, Lee-Young
通讯作者: Chau, Lee-Young
通过对心脏转录因子的非肌细胞进行重编程通过重编程。
DOI: 10.1038/nature11139
发表时间: 2012-05-13
期刊: NATURE
影响因子: 64.8
作者:
Song, Kunhua;Nam, Young-Jae;Luo, Xiang;Qi, Xiaoxia;Tan, Wei;Huang, Guo N.;Acharya, Asha;Smith, Christopher L.;Tallquist, Michelle D.;Neilson, Eric G.;Hill, Joseph A.;Bassel-Duby, Rhonda;Olson, Eric N.
通讯作者: Olson, Eric N.
DOI: 10.1016/j.cardfail.2009.01.013
发表时间: 2009-04
影响因子: 6
作者:
Jaski, Brian E.;Jessup, Mariell L.;Mancini, Donna M.;Cappola, Thomas P.;Pauly, Daniel F.;Greenberg, Barry;Borow, Kenneth;Dittrich, Howard;Zsebo, Krisztina M.;Hajjar, Roger J.
通讯作者: Hajjar, Roger J.
DOI: 10.1038/sj.onc.1207420
发表时间: 2004-04-29
期刊: ONCOGENE
影响因子: 8
作者:
EL Naaman, C;Grum-Schwensen, B;Ambartsumian, N
通讯作者: Ambartsumian, N
DOI: 10.1073/pnas.1109493108
发表时间: 2011-09-20
影响因子: 11.1
作者:
O'Connell, Joyce T.;Sugimoto, Hikaru;Kalluri, Raghu
通讯作者: Kalluri, Raghu