Study on the molecular mechanisms and treatment for mitochondrial regulation in cardiac remodeling

线粒体氧化应激导致线粒体DNA损伤的灾难性循环，以及功能衰退、更高的氧化应激和细胞损伤。氧化应激可激活多种肥大信号通路和转录因子，并介导细胞凋亡。它还刺激心脏成纤维细胞增殖，激活基质金属蛋白酶，导致细胞外基质重塑。这些细胞事件参与了适应性不良心肌重塑和衰竭的发生和发展。

Mitochondrial oxidative stress leads to a catastrophic cycle of mitochondrial DNA damage as well as functional decline, higher oxidative stress, and cellular injury. Oxidative stress activates a broad variety of hypertrophy signaling kinases and transcription factors and mediate apoptosis. It also stimulates cardiac fibroblast proliferation and activates the matrix metalloproteinases, leading to the extracellular matrix remodeling. These cellular events are involved in the development and progression of maladaptive myocardial remodeling and failure.