Skin may help reveal early changes that precede visible features of skin aging.
Evidence
This perspective review discusses human epidermal and full-thickness skin organoid models and emerging findings on protein folding, proteasomal activity, autophagy, sebocyte proteostasis, and inflammaging.
Caveat
The article synthesizes early model-system insights and emphasizes conceptual challenges and experimental limitations rather than reporting definitive intervention outcomes.
Simplified
The decline of is a central hallmark of aging, the earliest manifestations of which have remained difficult to capture in human tissues with conventional model systems. The skin is a continuously renewing and environmentally exposed organ offering a uniquely accessible window into aging biology. Skin organoid technologies allow for long-term culturing of human epidermal and full-thickness skin-like tissues that accurately recapitulate important aspects of cellular heterogeneity, spatial organization, and stem cell dynamics. In this perspective, we discuss how skin are beginning to reveal early proteostasis alterations-encompassing impaired protein folding, reduced proteasomal activity, and autophagy dysfunction-that precede overt structural and functional hallmarks of skin aging, with particular emphasis on underexplored regulators- sebaceous gland and sebocyte-specific proteostasis, autophagy, and inflammaging. We also highlight emerging insights, conceptual challenges, and experimental limitations, and outline future directions for integrating skin organoids with skin-on-a-chip, single-cell proteomics, and stress-reporting approaches to advance proteostasis-targeted interventions in skin aging.
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