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Iron Deficiency-Induced Hair Loss Is Associated with ROS-Mediated Disruption of Wnt/β-Catenin Signaling
Sang-Ah Kwon1, So Young Bu2, Yeon-Hee Kim3
1Department of Food and Nutrition, Yonsei University, Seoul 03722, Republic of Korea.
Nutrients
|July 28, 2026
Summary
Maternal iron deficiency in mice causes hair loss in pups by increasing oxidative stress and reducing Wnt/β-catenin signaling. Postnatal iron supplementation can reverse these effects, promoting hair regrowth.
Area of Science:
- Developmental biology
- Nutritional science
- Dermatology
Background:
- Maternal iron deficiency during gestation can impact offspring development and health.
- Iron deficiency in pregnant mice leads to hair loss in pups, but the underlying mechanisms are not well understood.
Purpose of the Study:
- To investigate the mechanisms by which maternal iron deficiency causes abnormal hair growth in offspring.
- To evaluate the efficacy of iron supplementation in reversing these hair growth abnormalities.
Main Methods:
- Pregnant mice were fed either a control or iron-deficient diet, with offspring continuing on the same diet.
- Hair loss and follicular morphology were assessed, and some offspring were supplemented with iron post-weaning.
- In vitro studies used human follicle dermal papilla cells treated with deferoxamine (DFO) to model iron deficiency.
Main Results:
- Iron-deficient offspring exhibited hair loss, smaller body size, and abnormal hair follicles, which improved with iron supplementation.
- Iron deficiency was associated with increased oxidative stress, reduced Wnt/β-catenin signaling, and elevated caspase-3, NF-κB, and TGF-β activation.
- In vitro, DFO treatment mimicked these effects, and N-acetylcysteine reversed alterations, indicating reactive oxygen species (ROS) mediate the hair loss.
Conclusions:
- Early-life iron deficiency impairs hair growth via increased ROS, suppressed Wnt/β-catenin signaling, and enhanced apoptosis.
- Postnatal iron supplementation can effectively reverse these iron deficiency-induced hair abnormalities.
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