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Fatty acid oxidation regulates cellular senescence by modulating the autophagy-SIRT1 axis
Seungyeon Yang1, Subin Moon1, Soojung Claire Hur2
1Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 06591; Institute for Aging and Metabolic Diseases, College of Medicine, The Catholic University of Korea, Seoul 06591; Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea.
BMB Reports
|September 7, 2023
Summary
Fatty acid oxidation (FAO) regulates cellular senescence, a key factor in aging. Inhibiting FAO induces senescence via the autophagy-SIRT1 pathway, independent of energy levels.
Area of Science:
- Cellular biology
- Metabolism
- Aging research
Background:
- Cellular senescence, a state of irreversible cell cycle arrest, is a hallmark of aging and contributes to age-related diseases.
- Metabolic alterations are intrinsically linked to the aging process and cellular dysfunction.
- Fatty acid oxidation (FAO) is a crucial metabolic pathway whose role in senescence is increasingly recognized.
Discussion:
- This study elucidates the mechanism by which FAO inhibition triggers cellular senescence.
- The findings highlight the interplay between FAO, autophagy, and SIRT1 in regulating senescence.
- The process is mediated by acetyl-CoA and is independent of cellular energy depletion.
Key Insights:
- Inhibition of FAO, pharmacologically or genetically, induces p53-dependent senescence in human fibroblasts.
- Enhancing FAO can suppress replicative senescence.
- Increased autophagosome formation due to FAO inhibition reduces SIRT1 levels, promoting senescence.
Outlook:
- Targeting the FAO-autophagy-SIRT1 axis may offer novel therapeutic strategies for age-related conditions.
- Further research could explore the therapeutic potential of modulating FAO in aging and senescence.
- Understanding this pathway could lead to interventions that promote healthy aging by managing cellular senescence.
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