PDF(Pubmed)
Abstract：
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.
摘要：
衰老是一个复杂的过程，其特征是许多细胞器的功能下降。影响老化过程的各种因素，比如染色体异常，表观遗传变化,端粒缩短，氧化应激，和线粒体功能障碍。线粒体功能障碍显著影响衰老，因为线粒体调节细胞能量，氧化平衡，和钙水平。线粒体的完整性是由线粒体自噬维持的，这有助于维持细胞内稳态，防止ROS产生，并防止mtDNA损伤。然而,钙摄取和氧化应激的增加可以破坏线粒体膜电位和通透性，导致凋亡级联。这种破坏导致自由基的产生增加，导致线粒体DNA突变的氧化修饰和积累，导致细胞功能障碍和衰老。线粒体功能障碍,由于结构和功能的变化，与年龄相关的退行性疾病有关。本文综述了线粒体功能障碍，它对衰老和年龄相关疾病的影响，以及通过靶向线粒体功能障碍的潜在抗衰老策略。
