Department of Pathophysiology, Prostate Diseases Prevention and Treatment Research Center, College of Basic Medical Sciences, Jilin University, NO.990 Qinghua Street, Changchun, Jilin, China.
Department of Pathology, Zhuzhou Central Hospital, Zhuzhou, Hunan, China.
Mol Cell Biochem. 2024 Jul;479(7):1571-1582. doi: 10.1007/s11010-023-04812-1. Epub 2023 Aug 17.
Cardiac hypertrophy is the main adaptive response of the heart to chronic loads; however, prolonged or excessive hypertrophy promotes myocardial interstitial fibrosis, systolic dysfunction, and cardiomyocyte death, especially aseptic inflammation mediated by NLRP3 inflammasome, which can aggravate ventricular remodeling and myocardial damage, which is an important mechanism for the progression of heart failure. Various cardiac overloads can cause mitochondrial damage. In recent years, the mitochondria have been demonstrated to be involved in the inflammatory response during the development of cardiac hypertrophy in vitro and in vivo. As the NLRP3 inflammasome and mitochondria are regulators of inflammation and cardiac hypertrophy, we explored the potential functions of the NLRP3 inflammasome and mitochondrial dysfunction in cardiac hypertrophy. In particular, we proposed that the induction of mitochondrial dysfunction in cardiomyocytes may promote NLRP3-dependent inflammation during myocardial hypertrophy. Further in-depth studies could prompt valuable discoveries regarding the underlying molecular mechanisms of cardiac hypertrophy, reveal novel anti-inflammatory therapies for cardiac hypertrophy, and provide more desirable therapeutic outcomes for patients with cardiac hypertrophy.
心肌肥厚是心脏对慢性负荷的主要适应性反应；然而，长期或过度的肥厚会促进心肌间质纤维化、收缩功能障碍和心肌细胞死亡，特别是由 NLRP3 炎性体介导的无菌性炎症，这会加重心室重构和心肌损伤，是心力衰竭进展的重要机制。各种心脏超负荷均可导致线粒体损伤。近年来，已证明线粒体参与了体外和体内心肌肥厚发展过程中的炎症反应。由于 NLRP3 炎性体和线粒体是炎症和心肌肥厚的调节剂，我们探讨了 NLRP3 炎性体和线粒体功能障碍在心肌肥厚中的潜在功能。特别是，我们提出，诱导心肌细胞线粒体功能障碍可能会在心肌肥厚期间促进 NLRP3 依赖性炎症。进一步的深入研究可能会揭示心肌肥厚的潜在分子机制方面的有价值的发现，为心肌肥厚的抗炎治疗提供新的方法，并为心肌肥厚患者带来更理想的治疗效果。
