Growth factor signaling for cardioprotection against oxidative stress-induced apoptosis.
Growth factor signaling for cardioprotection against oxidative stress-induced apoptosis.
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DOI：
10.1089/152308603770380043
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发表时间：
2003-12
影响因子：
6.6
通讯作者：
Yuichiro J. Suzuki
中科院分区：
文献类型：
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作者：
Yuichiro J. Suzuki
在各种临床情况下，如缺血-再灌注损伤和蒽环类药物化疗，心脏都会受到氧化应激的影响。心肌细胞的损失是心力衰竭的主要问题;因此，保护心肌细胞免于细胞死亡是重要的。各种生长因子，包括胰岛素样生长因子、肝细胞生长因子、内皮素-1、成纤维细胞生长因子和转化生长因子，已显示保护心脏免受氧化应激。生长因子介导的心肌保护机制可能与抑制心肌细胞凋亡有关。本文就生长因子介导的心肌细胞抗凋亡信号转导的分子机制作一综述。胰岛素样生长因子-1激活磷脂酰肌醇3' -激酶和细胞外信号调节激酶途径。最近的研究表明，加塔-4可能是内皮素-1和肝细胞生长因子介导的心肌细胞存活的重要介质。这些生长因子，以及介质的生长因子信号，可能是有用的治疗策略，对氧化应激诱导的心脏损伤。
The heart is subjected to oxidative stress during various clinical situations, such as ischemia-reperfusion injury and anthracycline chemotherapy. The loss of cardiac myocytes is the major problem in heart failure; thus, it is important to protect cardiac myocytes against cell death. Various growth factors, including insulin like growth factor, hepatocyte growth factor, endothelin-1, fibroblast growth factor, and transforming growth factor, have been shown to protect the heart against oxidative stress. The mechanism of growth factor-mediated cardioprotection may involve the attenuation of cardiac myocyte apoptosis. The present article summarizes the current knowledge on the molecular mechanisms of growth factor-mediated antiapoptotic signaling in cardiac myocytes. Insulin-like growth factor-1 activates phosphatidylinositol 3' -kinase and extracellular signal-regulated kinase pathways. Recent data showed that GATA-4 might be an important mediator of cardiac myocyte survival by endothelin-1 and hepatocyte growth factor. These growth factors, as well as mediators of growth factor-signaling, may be useful in therapeutic strategies against oxidative stress-induced cardiac injury.