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New insights into therole of mitochondriain aging:mitochondrialdynamics and more Arnold Y. SeoBertrand JosephDebapriya Dutta2010 год

New insights into the role of mitochondria in aging: mitochondrial dynamics and more
review

Страница публикацииПубликация в OpenAlex
Аннотация: A decline in mitochondrial function plays a key role in the aging process and increases the incidence of age-related disorders. A deeper understanding of the intricate nature of mitochondrial dynamics, which is described as the balance between mitochondrial fusion and fission, has revealed that functional and structural alterations in mitochondrial morphology are important factors in several key pathologies associated with aging. Indeed, a recent wave of studies has demonstrated the pleiotropic role of fusion and fission proteins in numerous cellular processes, including mitochondrial metabolism, redox signaling, the maintenance of mitochondrial DNA and cell death. Additionally, mitochondrial fusion and fission, together with autophagy, have been proposed to form a quality-maintenance mechanism that facilitates the removal of damaged mitochondria from the cell, a process that is particularly important to forestall aging. Thus, dysfunctional regulation of mitochondrial dynamics might be one of the intrinsic causes of mitochondrial dysfunction, which contributes to oxidative stress and cell death during the aging process. In this Commentary, we discuss recent studies that have converged at a consensus regarding the involvement of mitochondrial dynamics in key cellular processes, and introduce a possible link between abnormal mitochondrial dynamics and aging.
Год издания: 2010
Авторы: Arnold Y. Seo, Bertrand Joseph, Debapriya Dutta, Judy C.Y. Hwang, John P. Aris, Christiaan Leeuwenburgh
Издательство: The Company of Biologists
Источник: Journal of Cell Science
Ключевые слова: Mitochondrial Function and Pathology, Metabolism and Genetic Disorders, ATP Synthase and ATPases Research
Другие ссылки: Journal of Cell Science (HTML)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
PubMed (HTML)