Endocrine modulation of myofibroblast differentiation in skin wound healing: A systematic review and meta-analysis of preclinical models

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This systematic review explored how hormonal signaling affects myofibroblast activity during skin wound repair, drawing on data from both preclinical in vivo and in vitro experiments. The methodological quality of these studies was assessed using the SYRCLE risk of bias tool. We performed research in Scopus, PubMed/Medline, and Web of Science, selecting only primary research studies and following PRISMA recommendations. In animal models, lipid hormones, including 17-β estradiol, estrogen, and testosterone were found to enhance fibroblast differentiation, whereas dihydrotestosterone hindered this process by promoting pro-inflammatory cytokines and suppressing transforming growth factor beta (TGF-β) production through the mothers against decapentaplegic homolog 3 (AR-Smad3) pathway. Among peptide hormones, growth hormone (GH) raised insulin-like growth factor-1 (IGF-1) levels, intensified early inflammation, and reduced fibroblast-to-myofibroblast differentiation, as indicated by lower α-smooth muscle actin (α-SMA) levels. Growth hormone-releasing hormone (GHRH) decreased levels of inflammatory mediators such as cyclooxygenase-2 (COX-2) and promoted α-SMA expression, facilitating wound contraction. Similarly, glucagon-like peptide (GLP-1) and dexamethasone (DX) reduced inflammatory signaling and increased α-SMA, contributing to wound closure. The methodological quality of the included studies was heterogeneous, with frequent limitations related to reporting of randomization, allocation procedures, and outcome assessment. This review has been registered with PROSPERO (CRD42021264735).

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