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Does Calorie Restriction Modulate Inflammaging via FoxO Transcription Factors?
Sang-Eun Kim1, Ryoichi Mori1, Isao Shimokawa1
1Department of Pathology, School of Medicine and Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
Nutrients
|July 8, 2020
Summary
Calorie restriction (CR) extends lifespan by reducing inflammation and cellular senescence, potentially through FoxO3 transcription factors. This review explores CR
Area of Science:
- Aging research
- Molecular biology
- Immunology
Background:
- Calorie restriction (CR) extends lifespan and delays age-related decline in animals.
- Forkhead box O (FoxO) transcription factors (FoxO1, FoxO3) mediate CR's anti-neoplastic and lifespan-extending effects.
- Inflammaging, characterized by chronic low-grade inflammation, is linked to aging and diseases, with cellular senescence and NLRP3 inflammasome activation as key drivers.
Purpose of the Study:
- To review molecular mechanisms linking CR effects to inflammasome formation, focusing on FoxO3.
- To explore CR's role in attenuating inflammaging.
- To discuss neuroinflammation, adult neurogenesis, lifespan, and microRNA regulation in inflammaging.
Main Methods:
- Literature review of CR, FoxO transcription factors, inflammaging, cellular senescence, and NLRP3 inflammasome.
- Analysis of molecular pathways connecting CR and inflammasome activation.
- Inclusion of preliminary data from myeloid-specific Foxo1 and Foxo3 knockout mouse models.
Main Results:
- CR's anti-aging effects may be mediated by reducing inflammaging.
- FoxO transcription factors, particularly FoxO3, are central to CR's beneficial actions.
- Cellular senescence and NLRP3 inflammasome activation are implicated in CR's anti-inflammaging effects.
Conclusions:
- CR attenuates inflammaging, contributing to its lifespan-extending and health-promoting effects.
- FoxO3 is a key regulator linking CR, inflammation, and aging.
- Understanding these pathways offers therapeutic targets for age-related diseases.
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