ArticleThe American journal of sports medicine2026
Role of Hypoxia-Inducible Factor-1α in Regulating Muscle Degeneration After Rotator Cuff Tears.
Article in The American journal of sports medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSecondary muscle degeneration after a rotator cuff tear (RCT) critically affects clinical outcomes. Vascular compromise after a tendon injury creates a complex microenvironment that may be associated with the degeneration of rotator cuff muscle. The role of hypoxia-inducible factor-1α (HIF-1α), a master regulator of cellular stress responses to hypoxia, in modulating muscle abnormalities after an RCT remains undefined. PURPOSE: To define the role of HIF-1α in stem cell differentiation and muscle degeneration after an RCT in a murine model. STUDY
designControlled laboratory study.
methodsA supraspinatus tendon transection and suprascapular nerve transection (TTDN) model was established in C57BL/6J, platelet-derived growth factor receptor α (PDGFRα)-green fluorescent protein (GFP) reporter, and inducible cell-specific HIF-1α knockout mice. Vascularity and HIF-1α colocalization with fibroadipogenic progenitor (FAP) cells and satellite cells were analyzed. Fibrosis, fatty infiltration, and myofiber cross-sectional area were assessed. In vitro, HIF-1α was modulated in isolated FAP cells via CRISPR-Cas9 or prolyl hydroxylase domain inhibitors to evaluate FAP cell differentiation.
resultsTTDN induced significant capillary density reduction (CD31
conclusionAlthough vascularity was reduced after TTDN, pronounced global tissue hypoxia was not directly evidenced. Decreased global HIF-1α expression may reflect denervation-induced reductions in metabolic demand. HIF-1α emerges as a key player in FAP cell differentiation within the injury microenvironment, promoting brown adipose tissue differentiation and inhibiting fibrogenesis. CLINICAL RELEVANCE: Targeting HIF-1α in FAP cells offers a novel therapeutic strategy to mitigate secondary muscle atrophy and fibrosis after an RCT.
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