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Targeting Mitochondria as a Strategy to Inhibit Cellular Senescence

  • Molecular Biology of Cell Death and Aging (N Razdan and N Muhammad, Section Editors)
  • Published:
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Abstract

Purpose of Review

Cellular senescence is implicated in aging and age-related diseases. Because mitochondrial stress is one of the triggers of cellular senescence, and senescence leads to the accumulation of abnormal mitochondria with impaired dynamics and hampered homeostasis, this review focuses on the therapeutic potential of targeting mitochondria to quell senescence.

Recent Findings

Decreasing mitochondrial reactive oxygen species (ROS) production, balancing mitochondrial fusion and fission, increasing mitophagy, elevating mitochondrial NAD+ levels, and ensuring proper mitochondrial biogenesis prevent cells from becoming senescent. Regulating bioenergetics and mitochondrial calcium homeostasis also cause cell death in senescent cells.

Summary

Several interventions which modulate mitochondrial activities have now been developed to prevent the establishment of cellular senescence. However, recent studies also suggest that modulating mitochondrial homeostasis may kill senescent cells. Hence, more studies should also explore the possibility of targeting mitochondria as a strategy to eliminate senescent cells.

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Funding

Part of this work was supported by the Department of Science and Technology (DOST), National Academy of Science and Technology (NAST) (MCV).

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Authors and Affiliations

  1. Institute of Biology, College of Science, University of the Philippines, Regidor St., National Science Complex, Diliman, 1101, Quezon City, Philippines

    Irene L. Tan & Michael C. Velarde

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  1. Irene L. Tan
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  2. Michael C. Velarde
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Correspondence to Michael C. Velarde.

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This article is part of the Topical Collection on Molecular Biology of Cell Death and Aging

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Tan, I.L., Velarde, M.C. Targeting Mitochondria as a Strategy to Inhibit Cellular Senescence. Curr Mol Bio Rep 7, 20–29 (2021). https://doi.org/10.1007/s40610-021-00143-6

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