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Adjustment of the lysosomal-mitochondrial axis for control of cellular senescence

Adjustment of the lysosomal-mitochondrial axis for control of cellular senescence
Park, Joon TaeLee, Young-SamCho, Kyung A.Park, Sang Chul
DGIST Authors
Lee, Young-Sam
Issued Date
Article Type
AgingAutophagyLysosomal-mitochondrial axisLysosomeMitochondriaSenescence alleviation
Mitochondria and lysosomes undergo the most marked senescence-related alterations among all cellular organelles. Whereas mitochondria undergo gradual structural changes associated with reduced function, lysosomes exhibit progressively deteriorated function along with the accumulation of lipofuscins. Lysosomal dysfunction induces the deterioration of mitochondrial turnover, resulting in the generation of more reactive oxygen species (ROS), with the increased ROS levels in turn targeting lysosomes. This vicious feedback loop between lysosomes and mitochondria thus aggravates senescence phenotypes. Based on findings that lysosomal activity is diminished in senescent cells and that the resultant oxidative stress correlates with mitochondrial damage, the existence of a lysosomal–mitochondrial axis with a functional role in senescence has been proposed. In this review, we interrogate the interplay between lysosomes and mitochondria during senescence and propose the lysosomal-mitochondrial axis to serve a potential function as an inducer of senescence alleviation. Thus, learning how to control the lysosomal-mitochondrial axis should represent an important research directive for developing therapeutics toward ageing-related disease as well as the aging process itself. Further research focusing on the lysosomal-mitochondrial axis will add to our knowledge regarding aging and age-related pathologies, as well as provide new strategies for anti-aging intervention. © 2018 Elsevier B.V.
Elsevier Ireland Ltd
Related Researcher
  • 이영삼 Lee, Young-Sam 뉴바이올로지학과
  • Research Interests DNA replication and repair; Restoration of cellular senescence; Structural and functional relationship of proteins
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Department of New Biology Senescence-Associated Mechanism Lab 1. Journal Articles


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