ArticleFrontiers in immunology2026
Single-cell atlas of photoaged skin reveals JAK-STAT blockade as a strategy to reverse dermal remodeling.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Chronic ultraviolet (UV) exposure superimposes inflammatory and matrix-degenerative insults on intrinsic aging to produce cutaneous photoaging, yet the cell-type-resolved circuits and druggable nodes driving this process remain poorly defined. Methods: Chronic We established a chronic UVA+UVB-induced mouse model of photoaging and performed single-cell RNA sequencing of control, UV-exposed, and UV + ruxolitinib-treated dorsal skin to map photoaging and therapeutic response at cellular resolution. Results: Chronic Across 14 major lineages, UV exposure preserved overall cellular composition but induced a coordinated transcriptional network shift, marked by activation of JAK-STAT/IRF/AP-1-driven inflammatory and oxidative-stress programs and suppression of developmental, DNA-repair, and differentiation modules. Fibroblast reclustering resolved eight states and identified a papillary-to-reticular transitional continuum with the highest transcriptional burden, integrating senescence-associated secretory phenotype and extracellular-matrix disassembly signatures and skewing pseudotime toward late, terminal states. Topical JAK1/2 inhibition with ruxolitinib attenuated clinical and histological photoaging phenotypes, restored collagen and elastic fiber architecture, and rebalanced fibroblast trajectories by suppressing inflammatory/stress pathways while reactivating basement-membrane, extracellular-matrix, adhesion, and wound-healing programs. Cross-lineage analysis further revealed reversal of conserved stress-metabolic axes, including Discussion: Chronic These findings identify transitional fibroblasts as central executors of UV-driven dermal remodeling and support JAK1/2 inhibition as a network-level strategy to restore dermal-epidermal homeostasis in photoaged skin.
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