Please use this identifier to cite or link to this item: https://doi.org/10.1002/pmic.201800404
Title: Mitochondrial Dysfunction in Age-Related Metabolic Disorders
Authors: Natarajan, V 
Chawla, R 
Mah, T
Vivekanandan, R
Tan, SY 
Sato, PY
Mallilankaraman, K 
Keywords: aging
diabetes
metabolic diseases
mitochondrial calcium uniporter
mitochondrial dysfunction
mitophagy
obesity
Issue Date: 1-Mar-2020
Publisher: Wiley
Citation: Natarajan, V, Chawla, R, Mah, T, Vivekanandan, R, Tan, SY, Sato, PY, Mallilankaraman, K (2020-03-01). Mitochondrial Dysfunction in Age-Related Metabolic Disorders. Proteomics 20 (5-6) : e1800404-. ScholarBank@NUS Repository. https://doi.org/10.1002/pmic.201800404
Abstract: © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim 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.
Source Title: Proteomics
URI: https://scholarbank.nus.edu.sg/handle/10635/172704
ISSN: 16159853
16159861
DOI: 10.1002/pmic.201800404
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