Patil Ricky, Wang Hui, Kazaleh Matthew, Ailawadi Gorav, Salmon Morgan
Department of Cardiac Surgery, Michigan Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Frankel Cardiovascular Center, School of Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Pharmaceuticals (Basel). 2025 Jan 16;18(1):112. doi: 10.3390/ph18010112.
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.
线粒体功能障碍在血管疾病的发展中起核心作用,因为氧化应激会促进线粒体形态和功能的改变,进而导致疾病进展。氧化还原失衡会影响正常的细胞过程,包括线粒体生物发生、电化学平衡以及线粒体DNA的调控。在这篇综述中,我们将讨论这些失衡,特别是在线管疾病背景下线粒体融合、裂变、生物发生和线粒体自噬的潜在作用,以及正常功能的失调如何促进疾病进展。我们还将讨论将线粒体调节作为治疗靶点来治疗血管疾病形成的潜在意义。