A novel role for STAT3 in cardiac remodeling
A novel role for STAT3 in cardiac remodeling
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DOI：
10.1016/s1050-1738(01)00066-4
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发表时间：
2000-10-01
影响因子：
9.3
通讯作者：
Kishimoto, T
中科院分区：
文献类型：
--
作者：
Yamauchi-Takihara, K;Kishimoto, T
配体与gp 130的结合激活JAK/STAT信号转导途径，其中STAT 3在将信号从膜传递到细胞核中起核心作用。STAT 3在gp 130介导的心肌细胞肥大中起重要作用。心脏特异性破坏gp 130被证明是目前心力衰竭的机械应力伴随着细胞凋亡的增加。因此，由gp 130缺失导致的STAT 3失活可能是心脏肥大向心力衰竭转变的关键事件。适当的血管生长对于正常的心脏发育和重塑过程是必不可少的。近年来，bcl-xL和VEGF被认为是STAT的靶基因，它们共同作用可通过防止细胞凋亡和恢复能量剥夺来促进心肌细胞存活。在这篇综述中，STAT 3被强调为血管生成因子的调节剂，并提出了在心肌细胞中激活STAT介导的信号转导作为预防心力衰竭的新的治疗策略。（Trends Endovasc Med 2000; 10：298-303）。(C)2001年，爱思唯尔科学公司，
The binding of ligands to gp130 activates the JAK/STAT signal transduction pathway, where STAT3 plays a central role in transmitting signals from the membrane to the nucleus. STAT3 is essential for gp130-mediated cardiac myocte hypertrophy. Cardiac-specific disruption of gp130 was shown to present heart failure in response to mechanical stress accompanied by an increase in apoptosis. Thus, the inactivation of STAT3 resulting from the loss of gp130 may be a key event in the transition from cardiac hypertrophy to heart failure. Proper vascular growth is essential for normal cardiac development and remodeling process. Recently bcl-xL and VEGF have identified as target genes of STAT and together can promote cardiac myocyte survival by prevention of apoptosis and restoration of energy deprivation. In this review, STAT3 is highlighted as a regulator of angiogenic factors, and activation of STAT-mediated signaling in the cardiac myocyte is proposed as a novel therapeutic strategy for the prevention of heart failure. (Trends Cardiovasc Med 2000; 10:298-303). (C) 2001, Elsevier Science Inc,