Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Adipocytes as core drivers of skin aging and novel targets for regeneration.

Wang E., Xu Z., Wang Y., Wang J., Jiang Y., Zhao C.

Narrative Review on Skin Aging, published in Biogerontology (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Biogerontology (2026)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
41758428
DOI
10.1007/s10522-026-10413-4

Abstract (original English)

Skin aging has traditionally been attributed to alterations in the epidermis and dermis, including keratinocyte senescence, extracellular matrix (ECM) degradation, and fibroblast dysfunction. In contrast, the role of skin-associated adipose tissue (SAAT), particularly dermal white adipose tissue (dWAT), has been largely overlooked and considered a passive structural filler. Emerging evidence indicates that adipocyte aging is not merely a consequence of skin aging but may serve as a critical upstream driver that shapes the local microenvironment. Age-related functional decline of adipocytes, including the senescence-associated secretory phenotype (SASP), metabolic reprogramming, and altered adipokine secretion, can promote dermal ECM deterioration, perturb fibroblast function, and promote chronic low-grade inflammation. Furthermore, regional heterogeneity of dWAT across anatomical sites contributes to the spatial variability of skin aging patterns, influencing both the timing and severity of structural changes. Mechanistically, an adipocyte-immune-fibroblast tri-cellular network integrates signals from senescent adipocytes, immune cells, and fibroblasts, thereby amplifying tissue-level aging phenotypes. Current anti-aging interventions, which largely target epidermal or dermal compartments or focus on restoring tissue volume, often fail to address adipocyte dysfunction and its d

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
HumansSkin AgingAnimalsAdipocytesRegenerationCellular SenescenceFibroblastsSkin

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