What is it about?

This study investigates whether chlorogenic acid (CGA)—a natural polyphenol with known antioxidant and anti‑inflammatory properties—can protect adipocytes from stress‑induced cellular senescence. Using an in vitro model based on murine 3T3‑L1 adipocytes, senescence was triggered by oxidative stress, and the effects of CGA were evaluated by examining molecular markers of cell cycle arrest, inflammation, oxidative damage and impaired insulin signaling. CGA treatment restored key senescence‑related pathways, including Lamin B1 levels, the Bcl‑2/Bax ratio, and the modulation of p53, p21 and MAPK signaling. It also improved insulin signaling (PI3K‑AKT‑GLUT4 axis), glucose uptake, and reduced SASP‑associated inflammatory and extracellular matrix remodeling factors.

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Why is it important?

Cellular senescence contributes to adipose tissue dysfunction, inflammation and metabolic dysregulation, especially during aging. Identifying nutritional compounds capable of reducing senescence‑related alterations may help preserve adipocyte function. The findings show that CGA can attenuate multiple hallmarks of senescence in adipocytes, supporting its potential as a nutraceutical with senotherapeutic properties. This adds to the growing interest in dietary strategies aimed at counteracting age‑related declines in adipose tissue health.

Perspectives

These results position CGA as a promising candidate for strategies targeting senescence‑driven adipose dysfunction. Future research should include in vivo models and translational studies to confirm these effects and determine their relevance for metabolic disorders associated with aging. Further work may also clarify how CGA influences senescence‑related pathways under different stressors and in human adipocyte models.

Prof. Antonio Speciale
University of Messina

Read the Original

This page is a summary of: Effects of Chlorogenic Acid on Cellular Senescence in an In Vitro Model of 3T3-L1 Murine Adipocytes, Molecules, January 2026, MDPI AG,
DOI: 10.3390/molecules31010167.
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