Somasundaram Indumathi, Jain Samatha M, Blot-Chabaud Marcel, Pathak Surajit, Banerjee Antara, Rawat Sonali, Sharma Neeta Raj, Duttaroy Asim K
Biotechnology Engineering, Kolhapur Institute of Technology's College of Engineering, Kolhapur, India.
Department of Biotechnology, Faculty of Allied Health Sciences, Chettinad Hospital and Research Institute, Chettinad Academy of Research and Education, Chennai, India.
Front Physiol. 2024 Jul 2;15:1384966. doi: 10.3389/fphys.2024.1384966. eCollection 2024.
Aging is a complex process that features a functional decline in many organelles. Various factors influence the aging process, such as chromosomal abnormalities, epigenetic changes, telomere shortening, oxidative stress, and mitochondrial dysfunction. Mitochondrial dysfunction significantly impacts aging because mitochondria regulate cellular energy, oxidative balance, and calcium levels. Mitochondrial integrity is maintained by mitophagy, which helps maintain cellular homeostasis, prevents ROS production, and protects against mtDNA damage. However, increased calcium uptake and oxidative stress can disrupt mitochondrial membrane potential and permeability, leading to the apoptotic cascade. This disruption causes increased production of free radicals, leading to oxidative modification and accumulation of mitochondrial DNA mutations, which contribute to cellular dysfunction and aging. Mitochondrial dysfunction, resulting from structural and functional changes, is linked to age-related degenerative diseases. This review focuses on mitochondrial dysfunction, its implications in aging and age-related disorders, and potential anti-aging strategies through targeting mitochondrial dysfunction.
衰老 是一个复杂的过程,其特征是许多细胞器功能衰退。各种因素会影响衰老过程,如染色体异常、表观遗传变化、端粒缩短、氧化应激和线粒体功能障碍。线粒体功能障碍对衰老有显著影响,因为线粒体调节细胞能量、氧化平衡和钙水平。线粒体自噬维持线粒体的完整性,有助于维持细胞内稳态,防止活性氧生成,并保护线粒体DNA免受损伤。然而,钙摄取增加和氧化应激会破坏线粒体膜电位和通透性,导致凋亡级联反应。这种破坏会导致自由基产生增加,导致线粒体DNA突变的氧化修饰和积累,从而导致细胞功能障碍和衰老。由结构和功能变化引起的线粒体功能障碍与年龄相关的退行性疾病有关。本综述重点关注线粒体功能障碍、其在衰老和年龄相关疾病中的影响,以及通过针对线粒体功能障碍的潜在抗衰老策略。