Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Cardiovascular Research Institute of Wuhan University, Wuhan 430060, China.
Clin Sci (Lond). 2017 Aug 24;131(18):2319-2345. doi: 10.1042/CS20171167. Print 2017 Sep 15.
Cardiac remodelling is classified as physiological (in response to growth, exercise and pregnancy) or pathological (in response to inflammation, ischaemia, ischaemia/reperfusion (I/R) injury, biomechanical stress, excess neurohormonal activation and excess afterload). Physiological remodelling of the heart is characterized by a fine-tuned and orchestrated process of beneficial adaptations. Pathological cardiac remodelling is the process of structural and functional changes in the left ventricle (LV) in response to internal or external cardiovascular damage or influence by pathogenic risk factors, and is a precursor of clinical heart failure (HF). Pathological remodelling is associated with fibrosis, inflammation and cellular dysfunction (e.g. abnormal cardiomyocyte/non-cardiomyocyte interactions, oxidative stress, endoplasmic reticulum (ER) stress, autophagy alterations, impairment of metabolism and signalling pathways), leading to HF. This review describes the key molecular and cellular responses involved in pathological cardiac remodelling.
心脏重构可分为生理性(生长、运动和妊娠时)或病理性(炎症、缺血、缺血/再灌注(I/R)损伤、生物力学应激、神经激素过度激活和后负荷过度时)。心脏的生理性重构是以精细协调的方式进行的有益适应性改变过程。病理性心脏重构是指左心室(LV)对内部或外部心血管损伤或致病风险因素的影响做出的结构和功能改变,是临床心力衰竭(HF)的前期表现。病理性重构与纤维化、炎症和细胞功能障碍(如异常心肌细胞/非心肌细胞相互作用、氧化应激、内质网(ER)应激、自噬改变、代谢和信号通路受损)有关,可导致 HF。本文综述了病理性心脏重构中涉及的关键分子和细胞反应。