The role of mitochondria and mitophagy in cell senescence.

Autophagy Cell senescence Mitophagy Signaling pathways

Journal

Advances in protein chemistry and structural biology
ISSN: 1876-1631
Titre abrégé: Adv Protein Chem Struct Biol
Pays: Netherlands
ID NLM: 101497281

Informations de publication

Date de publication:
2023
Historique:
medline: 14 7 2023
pubmed: 13 7 2023
entrez: 12 7 2023
Statut: ppublish

Résumé

Mitochondrial malfunction and cell senescence have been defined as the hallmarks of aging. Cell senescence leads to the loss of health allied with aging. While deciphering the complex association between mitochondria and cellular senescence, it is observed that senescence has a two-faced nature being beneficial and hazardous. This duality of cellular senescence is associated with circumstantial aspects. During the process of cellular senescence, dysfunctional mitochondria are accumulated, the efficiency of the oxidative phosphorylation process declines along with the enhanced synthesis of reactive oxygen species. It is suggested that reduction in the negative consequences of senescence throughout old age might be accomplished by targeting the mitochondria as all roads lead towards mitochondria. It is unclear how perturbation of mitophagy in senescence results in the accumulation of mitochondria, impairment of mitochondrial biogenesis and onset of diseases. Understanding this complex interplay will bring about a long yet healthy lifespan. But definitely casual and specific players contribute in the initiation and conservation of the cell senescence. Variations in metabolism, quality control and dynamics of mitochondria are observed during cell aging process. Several On-target and Off-target mechanisms can also cause side effects in cellular senescence. Translational research of these mechanisms may lead to effective clinical interventions. This chapter reviews the role of mitochondria, homeostatic mechanisms and mitophagy as drivers and effectors of cell senescence along with multiple signalling pathways that lead to the initiation, maintenance, induction and suppression of cellular aging process during health and disease.

Identifiants

pubmed: 37437987
pii: S1876-1623(23)00043-3
doi: 10.1016/bs.apcsb.2023.03.001
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

93-115

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Auteurs

Tayyab Ali (T)

Clinico-Molecular Biochemistry Laboratory, Department of Biochemistry, Faculty of Sciences, University of Agriculture, Faisalabad, Pakistan.

Fatma Hussain (F)

Clinico-Molecular Biochemistry Laboratory, Department of Biochemistry, Faculty of Sciences, University of Agriculture, Faisalabad, Pakistan. Electronic address: fatmah@uaf.edu.pk.

Haroon Ur Rashid Kayani (HUR)

Department of Computer Science and Information Technology, University of Lahore, Sargodha Campus, Sargodha, Pakistan.

Muhammad Naeem (M)

College of Life Science, Hebei Normal University, Shijiazhuang, P.R. China.

Fozia Anjum (F)

Department of Chemistry, Government College University, Faisalabad, Pakistan.

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Classifications MeSH