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studies would be useful to support this outcome and better guide clinical antibiotic prescribing practices. Accumulation of excessive extracellular matrix (ECM) and aberrant transforming growth factor β (TGF-β) signaling pathway function can be potential therapeutic targets for keloid treatment. In this study, we examined the antifibrotic effect of metformin as a suppressor of TGF-β signaling pathways in human dermal fibroblasts (HDFs) and keloid spheroids. Human dermal fibroblasts were stimulated with TGF-β (10 ng/mL) and treated with m
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