线粒体DNA
粒线体疾病
氧化磷酸化
代谢综合征
线粒体融合
氧化应激
线粒体分裂
呼吸链
线粒体生物发生
医学
线粒体呼吸链
蛋白质组
生物化学
内科学
作者
Venkateswaran Natarajan,Ritu Chawla,Tania Ken Lin Mah,Rajesh Vivekanandan,Shu Tan,Priscila Y. Sato,Karthik Babu Mallilankaraman
出处
期刊:Proteomics
[Wiley]
日期:2020-03-01
卷期号:20 (5-6): e1800404-e1800404
被引量:81
标识
DOI:10.1002/pmic.201800404
摘要
Aging is a natural biological process in living organisms characterized by receding bioenergetics. Mitochondria are crucial for cellular bioenergetics and thus an important contributor to age-related energetics deterioration. In addition, mitochondria play a major role in calcium signaling, redox homeostasis, and thermogenesis making this organelle a major cellular component that dictates the fate of a cell. To maintain its quantity and quality, mitochondria undergo multiple processes such as fission, fusion, and mitophagy to eliminate or replace damaged mitochondria. While this bioenergetics machinery is properly protected, the functional decline associated with age and age-related metabolic diseases is mostly a result of failure in such protective mechanisms. In addition, metabolic by-products like reactive oxygen species also aid in this destructive pathway. Mitochondrial dysfunction has always been thought to be associated with diseases. Moreover, studies in recent years have pointed out that aging contributes to the decay of mitochondrial health by promoting imbalances in key mitochondrial-regulated pathways. Hence, it is crucial to understand the nexus of mitochondrial dysfunction in age-related diseases. This review focuses on various aspects of basic mitochondrial biology and its status in aging and age-related metabolic diseases.
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