PDF(Pubmed)
Abstract：
Cardiovascular diseases are caused by pathological cardiac remodeling, which involves fibrosis, inflammation and cell dysfunction. This includes autophagy, apoptosis, oxidative stress, mitochondrial dysfunction, changes in energy metabolism, angiogenesis and dysregulation of signaling pathways. These changes in heart structure and/or function ultimately result in heart failure. In an effort to prevent this, multiple cardiovascular outcome trials have demonstrated the cardiac benefits of sodium‑glucose cotransporter type 2 inhibitors (SGLT2is), hypoglycemic drugs initially designed to treat type 2 diabetes mellitus. SGLT2is include empagliflozin and dapagliflozin, which are listed as guideline drugs in the 2021 European Guidelines for Heart Failure and the 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America Guidelines for Heart Failure Management. In recent years, multiple studies using animal models have explored the mechanisms by which SGLT2is prevent cardiac remodeling. This article reviews the role of SGLT2is in cardiac remodeling induced by different etiologies to provide a guideline for further evaluation of the mechanisms underlying the inhibition of pathological cardiac remodeling by SGLT2is, as well as the development of novel drug targets.
摘要：
心血管疾病是由病理性心脏重塑引起的，涉及纤维化，炎症和细胞功能障碍。这包括自噬，凋亡，氧化应激，线粒体功能障碍，能量代谢的变化，血管生成和信号通路失调。心脏结构和/或功能的这些变化最终导致心力衰竭。为了防止这种情况，多项心血管结局试验证明了钠-葡萄糖协同转运蛋白2型抑制剂（SGLT2is）的心脏益处，最初设计用于治疗2型糖尿病的降血糖药物。SGLT2is包括empagliflozin和dapagliflozin，在2021年欧洲心力衰竭指南和2022年美国心脏协会/美国心脏病学会/美国心力衰竭学会心力衰竭管理指南中被列为指导药物。近年来,使用动物模型的多项研究探索了SGLT2is预防心脏重塑的机制.本文综述了SGLT2is在不同病因引起的心脏重塑中的作用，为进一步评估SGLT2is抑制病理性心脏重塑的机制提供了指导。以及新型药物靶点的开发。
