ArticleJournal of cachexia, sarcopenia and muscle2025
Iron Deficiency Impairs Muscle Stem Cell Proliferation and Skeletal Muscle Regeneration via HIF-2α Stabilization.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Is Ferroptosis the Mechanistic Bridge Connecting Iron Dysregulation to Muscle Wasting and Functional Decline in Aging?Aging cell · 2026Review
- Iron Deficiency Impairs Muscle Stem Cell Proliferation and Skeletal Muscle Regeneration via HIF-2α Stabilization.Journal of cachexia, sarcopenia and muscle · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundFunctional iron deficiency affects a large proportion of patients with chronic diseases and is increasingly observed in older adults. Clinical evidence links iron deficiency to sarcopenia, yet the mechanistic relationship between iron status and muscle regeneration remains poorly defined. This study investigates how iron depletion alters muscle stem cell (MuSC) proliferation and skeletal muscle regeneration, focusing on HIF-2α signalling.
methodsMale and female C57BL/6 J mice (4 week old, n > 20 per group in total) were fed iron-sufficient (IS) or iron-deficient (ID) chow for 4 weeks before cardiotoxin-induced tibialis anterior (TA) muscle injury. Muscle mass, MuSC proliferation and histological changes in regenerating TA muscles were evaluated at 10 and 30 days after injury (dpi). Pharmacological HIF-2α inhibition (PT2385) was used to determine causal mechanisms. Data were analyzed by t tests and one-way ANOVA.
resultsIron deficiency significantly reduced MuSC proliferation (-10.2% Ki67
conclusionsIron deficiency impairs skeletal muscle regeneration by stabilizing HIF-2α in MuSC, inducing Rb1 RNA expression, and repressing E2F-dependent proliferation. Transient HIF-2α inhibition rescues MuSC proliferation and muscle repair under iron-deficient conditions, highlighting HIF-2α as a potential therapeutic target to counteract sarcopenia in aging and chronic diseases.
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