Nutrients · 2026
Iron Deficiency-Induced Hair Loss Is Associated with ROS-Mediated Disruption of Wnt/β-Catenin Signaling.
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Kwon Sang-Ah, Bu So Young, Kim Yeon-Hee, Lim Joo Weon, Vulpe Christopher D, Lee Seung-Min
Аннотация
BACKGROUND: Gestational iron requirements may lead to maternal iron deficiency, increasing susceptibility in offspring. In mice, maternal iron deficiency induces hair loss in pups, but mechanisms remain poorly characterized.
OBJECTIVE: This study investigates mechanisms underlying maternal iron deficiency-induced abnormal hair growth and the impact of iron supplementation on pups' hair development.
METHODS: Pregnant C57BL/6J mice (nine-week-old, second week of gestation) were randomly assigned to a standard AIN-76 diet (control, CTRL) or an iron-deficient AIN diet (ID) until parturition and weaning. Offspring were maintained on the same diet as their mothers. At six weeks, hair loss was examined in one set (CTRL1 and ID), while the remaining were transitioned to an iron-replete AIN-76 diet (CTRL2 and IDN) for two additional weeks. An in vitro study with human follicle dermal papilla cells (HFDPC) via deferoxamine (DFO) treatment was performed.
RESULTS: ID offspring exhibited truncal hairlessness, reduced body size, and abnormal follicular morphology compared to CTRL1, while IDN demonstrated hair regrowth comparable to CTRL2. ID skin tissues had reduced Wnt/β-catenin signaling, elevated oxidative stress markers, and activation of caspase-3, nuclear factor kappa B (NF-κB), and transforming growth factor-beta (TGF-β) signaling, all reversed by iron supplementation. DFO-treated HFDPCs demonstrated increased cellular and mitochondrial reactive oxygen species (ROS), diminished Wnt/β-catenin signaling, activation of caspase-3, NF-κB, and TGF-β signaling pathways. N-acetylcysteine pretreatment abrogated DFO-induced alterations in Wnt/β-catenin signaling and apoptosis, suggesting ROS mediates iron deficiency-induced hair loss.
CONCLUSIONS: Early iron deficiency may have impaired hair growth through increased ROS production, reduced Wnt/β-catenin signaling, and enhanced apoptotic signals, while postnatal iron supplementation could reverse these abnormalities.
OBJECTIVE: This study investigates mechanisms underlying maternal iron deficiency-induced abnormal hair growth and the impact of iron supplementation on pups' hair development.
METHODS: Pregnant C57BL/6J mice (nine-week-old, second week of gestation) were randomly assigned to a standard AIN-76 diet (control, CTRL) or an iron-deficient AIN diet (ID) until parturition and weaning. Offspring were maintained on the same diet as their mothers. At six weeks, hair loss was examined in one set (CTRL1 and ID), while the remaining were transitioned to an iron-replete AIN-76 diet (CTRL2 and IDN) for two additional weeks. An in vitro study with human follicle dermal papilla cells (HFDPC) via deferoxamine (DFO) treatment was performed.
RESULTS: ID offspring exhibited truncal hairlessness, reduced body size, and abnormal follicular morphology compared to CTRL1, while IDN demonstrated hair regrowth comparable to CTRL2. ID skin tissues had reduced Wnt/β-catenin signaling, elevated oxidative stress markers, and activation of caspase-3, nuclear factor kappa B (NF-κB), and transforming growth factor-beta (TGF-β) signaling, all reversed by iron supplementation. DFO-treated HFDPCs demonstrated increased cellular and mitochondrial reactive oxygen species (ROS), diminished Wnt/β-catenin signaling, activation of caspase-3, NF-κB, and TGF-β signaling pathways. N-acetylcysteine pretreatment abrogated DFO-induced alterations in Wnt/β-catenin signaling and apoptosis, suggesting ROS mediates iron deficiency-induced hair loss.
CONCLUSIONS: Early iron deficiency may have impaired hair growth through increased ROS production, reduced Wnt/β-catenin signaling, and enhanced apoptotic signals, while postnatal iron supplementation could reverse these abnormalities.