Effects of Thyroid Dysfunction on Angiogenesis During Wound Healing and Skin Repair: A Systematic Review

TL;DR

This review explores how thyroid dysfunction affects blood vessel growth during skin wound healing and identifies potential treatments.

Contribution

The study systematically reviews the impact of thyroid dysfunction on angiogenesis and introduces novel therapeutic approaches.

Findings

Hypothyroidism reduces angiogenic activity and delays wound healing.

Hyperthyroidism increases neovascularization but may cause dysregulated remodeling.

Thyroxine-based therapies and exosomes show promise in enhancing wound angiogenesis.

Abstract

Thyroid hormones (THs) play an important role in regulating cellular metabolism and tissue homeostasis, particularly influencing angiogenesis, an essential component of wound healing. This systematic review evaluates the current evidence on how thyroid dysfunction, hypothyroidism and hyperthyroidism, impacts angiogenic processes during cutaneous wound repair. A comprehensive search across PubMed, Web of Science, and Scopus identified 61 candidate studies. After applying inclusion criteria focused on original research evaluating TH status and angiogenesis in skin wound models, 26 high-quality studies were included. Evidence demonstrates that hypothyroidism leads to diminished angiogenic activity, delayed re-epithelialization, and decreased expression of vascular markers such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α (HIF-1α). Conversely, hyperthyroid conditions showed enhanced neovascularization, although sometimes with dysregulated or excessive remodeling. Emerging experimental therapies, including thyroxine-impregnated biomaterials, nanofiber delivery systems, and stem cell-derived exosomes, also revealed promising angiogenic effects when modulated by THs. This review demonstrates the importance of thyroid status in wound care and highlights therapeutic opportunities for endocrine-modulated vascular repair.

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