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Updated: May 23, 2025

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MAPK15 controls mitochondrial fitness and contributes to prevent cellular senescence

Lorenzo Franci1, Giovanni Inzalaco1,2, Mario Chiariello1

  • 1Istituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR), and Core Research Laboratory (CRL), Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO), Siena, Italy.

Autophagy Reports
|May 21, 2025
PubMed

Insights

MAPK15 controls mitophagy, a process that removes damaged mitochondria. This prevents reactive oxygen species (ROS) buildup, DNA damage, and cellular senescence, impacting aging and cancer.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Dysfunctional mitochondria produce reactive oxygen species (ROS), causing oxidative stress and DNA damage.
  • Oxidative stress activates cellular senescence, which suppresses cancer but contributes to aging and age-related diseases.
  • Mitophagy is crucial for clearing damaged mitochondria and maintaining low intracellular ROS levels.

Purpose of the Study:

  • To investigate the role of the atypical MAP kinase MAPK15 in regulating mitophagy.
  • To understand how MAPK15 influences ROS accumulation, DNA damage, and cellular senescence.

Main Methods:

  • Investigated the function of MAPK15 in cellular models.
  • Assessed the impact of MAPK15 on mitochondrial health and ROS production.
  • Examined the relationship between MAPK15, mitophagy, and senescence pathways.

Main Results:

  • Identified MAPK15 as a key regulator of the mitophagic process.
  • Demonstrated that MAPK15 controls ROS accumulation and subsequent DNA damage.
  • Showed that MAPK15 activation prevents the induction of cellular senescence.

Conclusions:

  • MAPK15 plays a critical role in maintaining mitochondrial quality control through mitophagy.
  • By regulating mitophagy, MAPK15 mitigates oxidative stress, DNA damage, and cellular senescence.
  • Targeting MAPK15 may offer therapeutic strategies for age-related disorders and cancer prevention.
Keywords:
MAPKcell homeostasismitophagyoxidative stresssenescence

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