粒体自噬
线粒体融合
线粒体
背景(考古学)
氧化应激
线粒体生物发生
生物发生
医学
疾病
线粒体分裂
细胞生物学
线粒体DNA
DNAJA3公司
生物信息学
神经科学
生物
自噬
病理
遗传学
内分泌学
细胞凋亡
古生物学
基因
作者
Rasika Patil,Hui Wang,Matthew Kazaleh,Gorav Ailawadi,Morgan Salmon
出处
期刊:Pharmaceuticals
[Multidisciplinary Digital Publishing Institute]
日期:2025-01-16
卷期号:18 (1): 112-112
摘要
Mitochondria dysfunction plays a central role in the development of vascular diseases as oxidative stress promotes alterations in mitochondrial morphology and function that contribute to disease progression. Redox imbalances can affect normal cellular processes including mitochondrial biogenesis, electrochemical equilibrium, and the regulation of mitochondrial DNA. In this review, we will discuss these imbalances and, in particular, the potential role of mitochondrial fusion, fission, biogenesis, and mitophagy in the context of vascular diseases and how the dysregulation of normal function might contribute to disease progression. We will also discuss potential implications of targeting mitochondrial regulation as therapeutic targets to treat vascular disease formation.
科研通智能强力驱动
Strongly Powered by AbleSci AI