PDF(Pubmed)
Abstract：
Vascular smooth muscle cells (VSMCs) are integral to the pathophysiology of cardiovascular diseases (CVDs). Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, plays a crucial role in epigenetic regulation of VSMCs gene expression. Emerging researches suggest that EZH2 has a dual role in VSMCs, contingent on the pathological context of specific CVDs. This mini-review synthesizes the current knowledge on the mechanisms by which EZH2 regulates VSMC proliferation, migration and survival in the context of CVDs. The goal is to underscore the potential of EZH2 as a therapeutic target for CVDs treatment. Modulating EZH2 and its associated epigenetic pathways in VSMCs could potentially ameliorate vascular remodeling, a key factor in the progression of many CVDs. Despite the promising outlook, further investigation is warranted to elucidate the epigenetic mechanisms mediated by EZH2 in VSMCs, which may pave the way for novel epigenetic therapies for conditions such as atherosclerosis and hypertension.
摘要：
血管平滑肌细胞（VSMC）是心血管疾病（CVD）的病理生理学不可或缺的部分。zeste同源物2（EZH2）的增强子，组蛋白甲基转移酶,在VSMCs基因表达的表观遗传调控中起着至关重要的作用。新兴研究表明，EZH2在VSMC中具有双重作用，视特定CVD的病理背景而定。这篇小型综述综合了目前关于EZH2调节VSMC增殖的机制的知识，CVD背景下的迁移和生存。目标是强调EZH2作为CVD治疗的治疗靶标的潜力。在VSMC中调节EZH2及其相关的表观遗传途径可能会改善血管重塑，许多CVD进展的关键因素。尽管前景看好,有必要进一步研究以阐明VSMC中EZH2介导的表观遗传机制，这可能为动脉粥样硬化和高血压等疾病的新型表观遗传疗法铺平道路。
