Backgrouds and objective: Keloids are defined as overrepairing products that develop after skin lesions. Keloids are characterized by the proliferation of fibroblasts and the overaccumulation of extracellular matrix components (mainly collagen), leading to a locally hypoxic microenvironment. Hence, this article was aimed to review hypoxia in pathogenesis of keloids.
Methods: We reviewed and summarized the relevant published studies.
Results: Hypoxia results in the accumulation of hypoxia-inducible factor 1α (HIF-1α) in keloids, contributing to overactivation of the fibrotic signaling pathway, epithelial-mesenchymal transition, and changes in metabolism, eventually leading to aggravated fibrosis, infiltrative growth, and radiotherapy resistance.
Conclusion: It is, therefore, essential to understand the role of HIF-1α in the pathogenic mechanisms of keloids in order to develop new therapeutic approaches.
Keywords: Epithelial-Mesenchymal Transition; Fibrosis; HIF-1α; Hypoxia; Keloid.
© 2023 The Authors. Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.