ArticleCell cycle (Georgetown, Tex.)
M2 macrophages promote PKM2 production in fibroblasts to alleviate UVB-induced photoaging.
Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Leukocyte-Rich Platelet-Rich Plasma (L-PRP) Promotes Rejuvenation of Senescent Fibroblasts and Dermal Remodeling via CCL1-CCR8 Signaling and PKM2 Modulation.International journal of molecular sciences · 2026Article
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8 authors.
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Abstract
Ultraviolet radiation is a major factor in causing skin aging. Compared to younger individuals, older adults exhibit a significant imbalance in the M1/M2 macrophage ratio, with an elevated proportion of M1 macrophages, but little is known about the role of macrophages in skin aging. Here, we report the critical role of M2 macrophages and PKM2 in preventing fibroblast photoaging. UVB-treated photoaged fibroblasts showed a reduction in PKM2. Compared to M1 macrophages, treatment with M2 macrophage significantly alleviated this photoaging and enhanced PKM2 synthesis in fibroblasts. Mechanistically, this is due to the secretion of CCL1 by M2 macrophages, which acts on the CCR8 receptor on the cell surface, promoting PKM2 production in photoaged fibroblasts. This further activates the TGF-β1/Smad2 pathway, thereby reducing cellular aging. This provides a potential strategy for the treatment of skin photoaging.
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