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Updated: May 31, 2026

Induction and Validation of Cellular Senescence in Primary Human Cells
08:18

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Reduced Epidermal p21 Expression Is Identified in Some Subjects on Systemic GLP-1 Receptor Agonists: A

Saranya Wyles1, Shilpa Gopinath1, Brock Lynn1

  • 1Department of Dermatology, Mayo Clinic, Rochester, Minnesota.

Dermatologic Surgery : Official Publication for American Society for Dermatologic Surgery [Et Al.]
|May 29, 2026
PubMed
Abstract

Insights

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) may reduce skin aging by decreasing cellular senescence. This pilot study observed reduced epidermal p21 expression in participants using GLP-1RAs, suggesting a potential senomorphic effect.

Area of Science:

  • Dermatology
  • Gerontology
  • Metabolic Medicine

Background:

  • Cellular senescence is a key driver of skin aging.
  • Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have systemic metabolic and anti-inflammatory effects.
  • Human data on GLP-1RA effects on skin aging are limited.

Purpose of the Study:

  • To investigate if GLP-1RA therapy reduces cutaneous senescence.
  • To quantify senescence using epidermal p21 expression.
  • To assess clinical phenotypes with AI-driven facial imaging.

Main Methods:

  • A controlled observational pilot study with 3 male adults.
  • Punch biopsies from sun-protected gluteal sites to assess intrinsic aging.
  • Quantification of p21-positive nuclei in the epidermis and AI-based facial age estimation.

Main Results:

  • Reduced epidermal senescence observed in GLP-1RA users compared to a control.
  • Senescence burdens were 2.4% and 0.6% in GLP-1RA users versus 8.0% in the control.
  • AI facial age estimation correlated with chronological age.

Conclusions:

  • Systemic GLP-1RA exposure may reduce epidermal p21 expression.
  • This suggests a senomorphic effect of GLP-1RAs on skin.
  • Further studies are warranted to explore the link between metabolic regulation and skin aging.

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