Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence

Mitochondria are one of organelles that undergo significant changes associated with senescence. An increase in mitochondrial size is observed in senescent cells, and this increase is ascribed to the accumulation of dysfunctional mitochondria that generate excessive reactive oxygen species (ROS). Suc...

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Main Authors: Yun Haeng Lee, Ji Yun Park, Haneur Lee, Eun Seon Song, Myeong Uk Kuk, Junghyun Joo, Sekyung Oh, Hyung Wook Kwon, Joon Tae Park, Sang Chul Park
Format: Article
Language:English
Published: MDPI AG 2021-11-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/10/11/3003
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author Yun Haeng Lee
Ji Yun Park
Haneur Lee
Eun Seon Song
Myeong Uk Kuk
Junghyun Joo
Sekyung Oh
Hyung Wook Kwon
Joon Tae Park
Sang Chul Park
author_facet Yun Haeng Lee
Ji Yun Park
Haneur Lee
Eun Seon Song
Myeong Uk Kuk
Junghyun Joo
Sekyung Oh
Hyung Wook Kwon
Joon Tae Park
Sang Chul Park
author_sort Yun Haeng Lee
collection DOAJ
description Mitochondria are one of organelles that undergo significant changes associated with senescence. An increase in mitochondrial size is observed in senescent cells, and this increase is ascribed to the accumulation of dysfunctional mitochondria that generate excessive reactive oxygen species (ROS). Such dysfunctional mitochondria are prime targets for ROS-induced damage, which leads to the deterioration of oxidative phosphorylation and increased dependence on glycolysis as an energy source. Based on findings indicating that senescent cells exhibit mitochondrial metabolic alterations, a strategy to induce mitochondrial metabolic reprogramming has been proposed to treat aging and age-related diseases. In this review, we discuss senescence-related mitochondrial changes and consequent mitochondrial metabolic alterations. We assess the significance of mitochondrial metabolic reprogramming for senescence regulation and propose the appropriate control of mitochondrial metabolism to ameliorate senescence. Learning how to regulate mitochondrial metabolism will provide knowledge for the control of aging and age-related pathologies. Further research focusing on mitochondrial metabolic reprogramming will be an important guide for the development of anti-aging therapies, and will provide novel strategies for anti-aging interventions.
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spelling doaj.art-4e96e9a99cc243098ba18136314fbdac2023-11-22T22:49:52ZengMDPI AGCells2073-44092021-11-011011300310.3390/cells10113003Targeting Mitochondrial Metabolism as a Strategy to Treat SenescenceYun Haeng Lee0Ji Yun Park1Haneur Lee2Eun Seon Song3Myeong Uk Kuk4Junghyun Joo5Sekyung Oh6Hyung Wook Kwon7Joon Tae Park8Sang Chul Park9Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDepartment of Medical Sciences, Catholic Kwandong University College of Medicine, Incheon 22711, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaDivision of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, KoreaThe Future Life & Society Research Center, Chonnam National University, Gwangju 61186, KoreaMitochondria are one of organelles that undergo significant changes associated with senescence. An increase in mitochondrial size is observed in senescent cells, and this increase is ascribed to the accumulation of dysfunctional mitochondria that generate excessive reactive oxygen species (ROS). Such dysfunctional mitochondria are prime targets for ROS-induced damage, which leads to the deterioration of oxidative phosphorylation and increased dependence on glycolysis as an energy source. Based on findings indicating that senescent cells exhibit mitochondrial metabolic alterations, a strategy to induce mitochondrial metabolic reprogramming has been proposed to treat aging and age-related diseases. In this review, we discuss senescence-related mitochondrial changes and consequent mitochondrial metabolic alterations. We assess the significance of mitochondrial metabolic reprogramming for senescence regulation and propose the appropriate control of mitochondrial metabolism to ameliorate senescence. Learning how to regulate mitochondrial metabolism will provide knowledge for the control of aging and age-related pathologies. Further research focusing on mitochondrial metabolic reprogramming will be an important guide for the development of anti-aging therapies, and will provide novel strategies for anti-aging interventions.https://www.mdpi.com/2073-4409/10/11/3003mitochondrial metabolic reprogrammingmitochondriaROSsenescence amelioration
spellingShingle Yun Haeng Lee
Ji Yun Park
Haneur Lee
Eun Seon Song
Myeong Uk Kuk
Junghyun Joo
Sekyung Oh
Hyung Wook Kwon
Joon Tae Park
Sang Chul Park
Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
Cells
mitochondrial metabolic reprogramming
mitochondria
ROS
senescence amelioration
title Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
title_full Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
title_fullStr Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
title_full_unstemmed Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
title_short Targeting Mitochondrial Metabolism as a Strategy to Treat Senescence
title_sort targeting mitochondrial metabolism as a strategy to treat senescence
topic mitochondrial metabolic reprogramming
mitochondria
ROS
senescence amelioration
url https://www.mdpi.com/2073-4409/10/11/3003
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