Caturano Alfredo, Vetrano Erica, Galiero Raffaele, Salvatore Teresa, Docimo Giovanni, Epifani Raffaella, Alfano Maria, Sardu Celestino, Marfella Raffaele, Rinaldi Luca, Sasso Ferdinando Carlo
Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", I-80138 Naples, Italy.
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", I-80138 Naples, Italy.
Rev Cardiovasc Med. 2022 May 6;23(5):165. doi: 10.31083/j.rcm2305165. eCollection 2022 May.
Cardiac hypertrophy develops in response to increased workload to reduce ventricular wall stress and maintain function and efficiency. Pathological hypertrophy can be adaptive at the beginning. However, if the stimulus persists, it may progress to ventricular chamber dilatation, contractile dysfunction, and heart failure, resulting in poorer outcome and increased social burden. The main pathophysiological mechanisms of pathological hypertrophy are cell death, fibrosis, mitochondrial dysfunction, dysregulation of -handling proteins, metabolic changes, fetal gene expression reactivation, impaired protein and mitochondrial quality control, altered sarcomere structure, and inadequate angiogenesis. Diabetic cardiomyopathy is a condition in which cardiac pathological hypertrophy mainly develop due to insulin resistance and subsequent hyperglycaemia, associated with altered fatty acid metabolism, altered calcium homeostasis and inflammation. In this review, we summarize the underlying molecular mechanisms of pathological hypertrophy development and progression, which can be applied in the development of future novel therapeutic strategies in both reversal and prevention.
心脏肥大是对工作量增加的一种反应，目的是降低心室壁应力并维持功能和效率。病理性肥大起初可能具有适应性。然而，如果刺激持续存在，它可能进展为心室腔扩张、收缩功能障碍和心力衰竭，导致预后较差并增加社会负担。病理性肥大的主要病理生理机制包括细胞死亡、纤维化、线粒体功能障碍、离子处理蛋白失调、代谢变化、胎儿基因表达重新激活、蛋白质和线粒体质量控制受损、肌节结构改变以及血管生成不足。糖尿病性心肌病是一种主要由于胰岛素抵抗和随后的高血糖导致心脏病理性肥大的疾病，与脂肪酸代谢改变、钙稳态改变和炎症有关。在这篇综述中，我们总结了病理性肥大发生和进展的潜在分子机制，这些机制可应用于未来逆转和预防新型治疗策略的开发。
