MOLECULAR CROSSTALK BETWEEN IRON DEFICIENCY AND HAIR FOLLICLE INTEGRITY: A COMPREHENSIVE MECHANISTIC REVIEW
Keywords:
Iron deficiency; hair follicle; oxidative stress; mitochondrial dysfunction; telogen effluvium.Abstract
Despite investigating the role of iron in non-scarring alopecia, a number of molecular and cellular mechanisms are still unclear. Iron deficiency and iron overload affect cellular processes, including mitochondrial respiration, cellular redox homeostasis, oxidative stress, and hormone synthesis. To regulate iron homeostasis, body tightly shifts iron import/export via the hepcidin-ferroprotein axis. Detection of DNA and RNA with iron-responsive element/iron-regulatory protein system is another known mechanism. Connective tissue growth factor (CTGF) expression was downregulated in iron-depleted human fibroblasts. In hyperplastic Fxn-/- mice, iron deficiency was reported to exacerbate CTGF and TGF-β, leading to excessive fibroblast production and reduced vessel maturation. Also, Jansen et al. reported that iron depletion reduced the proliferation of normal cultured human fibroblasts. Decreased hematopoietic iron noticed in the absence of iron overload led to decreased hemoglobin synthesis in iron-deficient zebrafish, resulting in vasculogenesis failure.
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