Wincewicz Andrzej, Sulkowski Stanisław
Specialist Medical Practice-Pathologist, Non-Public Health Care Unit, Department of Pathology, Kielce, Poland.
Department of General Pathomorphology, Medical University of Bialystok, Poland.
Adv Clin Exp Med. 2017 Jul;26(4):703-708. doi: 10.17219/acem/62693.
The roles of STAT (signal transducers and activators of transcription) proteins are widely discussed in relation to other agents like IFN-γ that are involved in cardiovascular diseases. STAT3 protects cardiomyocytes during endotoxic shock and ischemia and prolongs survival of these cells by activation of antiapoptotic genes like Bcl-2 and c-Fos. Moreover, IL-6 dependent expression of STAT3 is probably responsible for hypertrophy of cardiomyocytes. On the contrary, STAT1 mediates cell death by induction of caspase-1. STAT6 probably enhances cellular damage in myocardial infraction, which is significantly reduced in mice with the knockout STAT6 gene. Considering these facts, we attempted to review in this paper the role of STAT proteins in myocardial remodeling, highlighting STAT3 as a potent mediator of cardioprotection. Our review also aims to acquaint a broad audience of internal medicine practitioners with the STAT3-related molecular mechanisms that underlie the therapeutic properties of such widely administered drugs as angiotensin II type 1 (AT1) receptor antagonists and HMG-CoA reductase inhibitors, such as losartan and lovastatin.
信号转导子和转录激活子（STAT）蛋白的作用在与心血管疾病相关的其他因子（如干扰素-γ）方面得到了广泛讨论。在内毒素休克和缺血期间，STAT3保护心肌细胞，并通过激活抗凋亡基因（如Bcl-2和c-Fos）延长这些细胞的存活时间。此外，STAT3的白细胞介素-6依赖性表达可能是心肌细胞肥大的原因。相反，STAT1通过诱导半胱天冬酶-1介导细胞死亡。STAT6可能会加重心肌梗死中的细胞损伤，而在敲除STAT6基因的小鼠中，这种损伤会显著减轻。考虑到这些事实，我们试图在本文中综述STAT蛋白在心肌重塑中的作用，强调STAT3是心脏保护的有效介质。我们的综述还旨在让广大内科医生了解与STAT3相关的分子机制，这些机制是1型血管紧张素II（AT1）受体拮抗剂和HMG-CoA还原酶抑制剂（如氯沙坦和洛伐他汀）等广泛使用药物治疗特性的基础。
