Hormonal Modulation of Cutaneous Wound Healing
Summary
Cutaneous wound healing is an intricate process encompassing haemostasis, inflammation, proliferation and remodelling. Hormones act at multiple stages to orchestrate cellular behaviours, extracellular matrix deposition and vascular responses. Oestrogens accelerate inflammatory resolution and promote re-epithelialisation by modulating cytokine networks and growth-factor signalling. Androgens, by contrast, may delay repair through prolongation of inflammation and reduction of angiogenic signals. Glucocorticoids exert potent anti-inflammatory effects but can impair fibroblast function and collagen synthesis when chronically elevated. Thyroid hormones influence keratinocyte proliferation and extracellular matrix turnover, while insulin and insulin-like growth factors support cellular metabolism and granulation-tissue formation. Emerging evidence also highlights the role of peptide hormones and neurohormones in fine-tuning wound-bed dynamics. Alterations in systemic hormone levels, such as oestrogen deficiency in menopause or stress-induced cortisol elevation, can result in delayed healing and chronic wound formation. Therapeutic strategies that harness or mimic these modulatory effects are under active investigation. Topical and systemic delivery of oestrogens has shown promise in restoring regenerative capacity in aged or hormone-deficient skin, while analogue design aims to minimise systemic side effects. Novel biomaterial carriers and controlled-release systems seek to localise hormonal activity to the wound environment. Understanding the balance and timing of hormonal signals is critical for developing targeted interventions that enhance repair without compromising tissue integrity or function.
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Hormonal Modulation of Cutaneous Wound Healing publication trend
The graph below shows the total number of articles in hormonal modulation of cutaneous wound healing across all publications each year (not limited to Nature Index journals).
Technical terms
Re-epithelialisation: Restoration of the epidermal layer by keratinocyte migration and proliferation.
Myofibroblast: Contractile cell type that secretes extracellular matrix and contributes to wound contraction.
Oestrogen receptor α (ERα): Nuclear receptor mediating genomic and non-genomic effects of oestrogens in target cells.
Angiogenesis: Formation of new blood vessels from existing vasculature, essential for nutrient delivery during healing.
Cytokine: Small secreted protein that modulates cell communication, inflammation and tissue repair.
References
- Hormonal interventions in skin wounds – a mini review. Molecular Medicine (2024).
- The different natural estrogens promote endothelial healing through distinct cell targets. JCI Insight (2023).
- Evaluation of Effects of Topical Estradiol Benzoate Application on Cutaneous Wound Healing in Ovariectomized Female Mice. PLOS ONE (2016).
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