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자료유형
학술저널
저자정보
황은성 (서울시립대학교) 황성윤 (서울시립대학교)
저널정보
대한노인병학회 Annals of geriatric medicine and research Annals of geriatric medicine and research Vol.21 No.4
발행연도
2017.1
수록면
149 - 157 (9page)

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The quality of mitochondria is a key determinant of mitochondrial ATP production and reactive oxygen species generation; therefore, it plays critical roles in energy homeostasis and cellular health. Mitochondrial quality is governed by mitochondrial turnover, which involves autophagic removal of old mitochondria and biogenesis of new ones. Both activities are critically modulated by sirtuin proteins, in particular, SIRT1 and SIRT3. These proteins activate mitophagy and mitochondrial biogenesis through deacetylation-mediated activation of factors participating in key steps of autophagy and mitochondrial protein expression. They also control other factors involved in maintenance of mitochondrial integrity and in damage prevention. At the same time, the activities and protein levels of SIRT1 and SIRT3 decline during aging, contributing to mitochondrial dysfunction associated with tissue aging and many degenerative diseases. However, recent studies suggest that the activity of the sirtuin proteins can be elevated through modulation of nicotinamide adenine dinucleotide (NAD+) and in physiological settings. An understanding of the underlying molecular pathways is actively sought and practical strategies are proposed based on basic research; nevertheless, their applicability at the clinical and subclinical levels could be better recognized and understood in the field of medicine. To this end, this review discusses the recent understanding of the biochemistry underlying the NAD+-redox mediated modulation of cellular sirtuin activity.

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