Tang Hong-Xia, Qin Xu-Ping, Li Jie
The First People's Hospital of Chenzhou, Institute of Pharmacy and Pharmacology, University of South China, Hunan, China.
School of Pharmacy, Southern Medical University, Guangdong, China.
Vascular. 2020 Dec;28(6):821-828. doi: 10.1177/1708538120929504. Epub 2020 Jun 2.
Cardiovascular disease (CVD) remains the primary cause of morbidity and mortality worldwide. The abnormal proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of CVD. The functional and phenotypic changes in vascular cells are mediated by complex signaling cascades that initiate and control genetic reprogramming. Many studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) regulates a diverse array of functions relevant to atherosclerosis.
In this review, we summarize the studies on the STAT3-mediated proliferation of VSMCs and subsequent CVDs such as hypertension, atherosclerosis, stroke, coronary artery disease, and myocardial infarction. Furthermore, we describe the general background of STAT3, its structure, function and regulation as well as the STAT3 signaling pathway. Finally, we highlight some potential issues and propose some solutions to these issues. STAT3 activation promotes the proliferation of VSMCs by regulating the transcription of genes. Studying the mechanism of VSMC proliferation induced by the STAT3 pathway is valuable for finding therapeutic targets for CVD.
心血管疾病（CVD）仍然是全球发病和死亡的主要原因。血管平滑肌细胞（VSMC）的异常增殖是心血管疾病发病机制中的关键事件。血管细胞的功能和表型变化由启动和控制基因重编程的复杂信号级联介导。许多研究表明，信号转导和转录激活因子3（STAT3）调节与动脉粥样硬化相关的多种功能。
在本综述中，我们总结了关于STAT3介导的VSMC增殖以及随后的心血管疾病（如高血压、动脉粥样硬化、中风、冠状动脉疾病和心肌梗死）的研究。此外，我们描述了STAT3的一般背景、其结构、功能和调节以及STAT3信号通路。最后，我们强调了一些潜在问题并提出了针对这些问题的一些解决方案。STAT3激活通过调节基因转录促进VSMC增殖。研究STAT3途径诱导VSMC增殖的机制对于寻找心血管疾病的治疗靶点具有重要价值。
