改变心室收缩力或促进心肌细胞肥大的心脏保护反应往往发生于心脏工作负荷增加(例如高血压)的情况下。当这种反应过度时,病理性心脏重塑出现,并促进心力衰竭的发展。关于这种反应的潜在机制目前尚未被全面阐述清楚。Tian等发现,血管生成素样蛋白2(ANGPLT2)在病理性重塑的小鼠和人心脏中表达增加,而在耐力训练诱导的小鼠生理性心脏重塑中 Cardioprotective responses that alter ventricular contractile force or promote cardiomyocyte hypertrophy often occur with increased cardiac workload (such as hypertension). When this reaction is over, pathological cardiac remodeling occurs and promotes the development of heart failure. The underlying mechanism for this response has not yet been fully articulated. Tian et al. Found that angiopoietin-like protein 2 (ANGPLT2) is expressed in pathologically remodeled mice and human hearts, whereas in endurance training-induced physiological cardiac remodeling in mice