医学
发病机制
线粒体
腹主动脉瘤
线粒体呼吸链
疾病
生物信息学
线粒体融合
主动脉瘤
线粒体DNA
病理
动脉瘤
细胞生物学
生物
外科
遗传学
基因
作者
Wenfan Yang,Jianxiong He,Hao Yu,Ya Wu,Sen Shi
标识
DOI:10.2174/0115701611312293241220101556
摘要
Abdominal Aortic Aneurysm (AAA) is a life-threatening vascular disease. Despite advancements in understanding the pathogenesis of AAA, significant knowledge gaps persist. Recent evidence increasingly implicates mitochondrial dysfunction as a contributing factor that exacerbates AAA, inducing further expansion of aneurysm, rupture, and subsequent death. This review summarizes the latest research findings and theories associated with AAA pathogenesis, with a particular focus on mitochondrial dysfunction in AAA, including mitochondrial quality control, mitochondrial membrane potential, mitochondrial morphology, oxidation and antioxidation, normal functioning of the respiratory chain, mitochondrial mutations, and the regulation of other mitochondrial signaling pathways. Moreover, we highlight potential medical interventions based on regulating mitochondrial function for AAA treatment.
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