The British journal of dermatologyDec 26, 2025

Problems with cell cleanup in aging skin cells linked to pale skin, improved by metformin

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 27, 2026

Abstract

Essence

ATG7 loss appears to be an early autophagy defect in melanocyte senescence, and metformin delayed this aging program in experimental melanocytes.

Evidence

Single-cell and time-course transcriptomic analyses of UVB-induced senescent melanocytes, supported by assays, immunohistochemistry, and ATG7 knockdown or overexpression, identified ATG7 downregulation in senescent melanocytes and idiopathic guttate hypomelanosis skin and showed metformin restored autophagy and redox balance.

Caveat

The intervention evidence comes from senescent melanocyte models rather than a clinical trial in people with hypopigmentary disorders.

Simplified

BACKGROUND: Melanocyte senescence predominantly occurs in sun-exposed skin of elderly individuals and contributes to skin aging and hypopigmentary disorders.

OBJECTIVES: To identify early molecular events preceding melanocyte senescence and to evaluate a therapeutic strategy for preventing melanocyte aging.

METHODS: Single-cell RNA sequencing and time-course bulk transcriptome analyses were performed on UVB-induced senescent melanocytes to identify senescence-associated pathways. Autophagy impairment was validated using gene and protein assays, immunohistochemistry, and ATG7 knockdown or overexpression. The protective effects of metformin on ATG7-dependent autophagy and redox balance were assessed in senescent melanocytes.

RESULTS: Autophagy dysregulation was identified as an early event preceding glycolytic reprogramming during UV-induced melanocyte senescence. ATG7 downregulation emerged as the earliest molecular alteration and was consistently observed in both senescent melanocytes and idiopathic guttate hypomelanosis skin. Metformin treatment restored autophagic activity, including ATG7 upregulation, and mitigated oxidative stress, thereby delaying melanocyte senescence.

CONCLUSION: Early autophagy dysfunction represents a key initiating event in melanocyte senescence. Autophagy preservation particularly through ATG7 maintenance offers a promising early intervention strategy to prevent melanocyte aging and related hypopigmentary disorders.

Full Text

Full text is available at the source.

View Full Text ↗

Featured in

Longevity & AgingIssue #17

Your fat tissue drives whole-body aging, while centenarians have lower nutritional scores than expected

↗

Problems with cell cleanup in aging skin cells linked to pale skin, improved by metformin

Abstract

Full Text

Featured in

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the longevity & aging brief