ArticleFrontiers in immunology2025
METTL3-mediated m6A modification regulates D-galactose-induced skin fibroblast senescence through miR-208a-5p.
Article in Frontiers in immunology, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Dual modes of action: direct regulation and ceRNA-mediated mechanisms of ncRNAs in dermal fibroblast senescence.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
11 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: As the most abundant epitranscriptomic modification, N6-methyladenosine (m6A) critically influences aging and age-related pathologies. However, its regulatory interplay with microRNAs (miRNAs) in skin aging remains poorly defined. Methods: Aging phenotypes were recapitulated using D-galactose (D-gal)-induced senescence models in mouse skin fibroblasts (MSFs) and mice. Interventions included METTL3 overexpression/knockdown, miR-208a-5p mimic/inhibitor transfection, and pharmacological mitophagy induction (GSK). Molecular analyses assessed m⁶A dynamics, gene regulation, and mitochondrial function. Results: In D-gal-induced aging models, global RNA hypomethylation and reduced METTL3 expression were observed, while METTL3 overexpression attenuated cellular senescence. Mechanistically, METTL3 depletion elevated miR-208a-5p levels via YTHDF2-mediated m⁶A recognition, establishing epitranscriptional control. This upregulated miR-208a-5p directly targeted the 3'-UTR of OPA1 (optic atrophy type 1), suppressing mitophagic activity. Critically, senescent phenotypes induced by METTL3 knockdown or miR-208a-5p mimicry were reversed by pharmacological mitophagy induction (GSK), confirming mitochondrial homeostasis as the pathway's functional nexus. Discussion: These results establish an m6A-dependent METTL3/miR-208a-5p/OPA1 axis that regulates mitophagy and skin aging. Pharmacological rescue of mitophagy highlights this pathway's therapeutic relevance for age-related dermatopathology.
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