{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T18:14:32Z","timestamp":1793297672335,"version":"4.5.0"},"reference-count":89,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"831","funder":[{"DOI":"10.13039\/100012067","name":"Babraham Institute","doi-asserted-by":"publisher","award":["UKRI-BBSRC"],"award-info":[{"award-number":["UKRI-BBSRC"]}],"id":[{"id":"10.13039\/100012067","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001711","name":"Swiss National Science Foundation","doi-asserted-by":"publisher","award":["CRSII- 222774"],"award-info":[{"award-number":["CRSII- 222774"]}],"id":[{"id":"10.13039\/501100001711","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003006","name":"Eidgen\u00f6ssische Technische Hochschule Z\u00fcrich","doi-asserted-by":"publisher","award":["ETH-24 19-1"],"award-info":[{"award-number":["ETH-24 19-1"]}],"id":[{"id":"10.13039\/501100003006","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2026,1,7]]},"abstract":"<jats:p>\n                    Tendons are sparsely vascularized connective tissues that link muscles to bones, withstanding some of the highest mechanical stresses in the body. Mechanical overloading and tissue hypervascularity are implicated in tendinopathy, a common musculoskeletal disorder, yet their mechanistic roles remain unclear. Here, we identify hypoxia-inducible factor 1\u03b1 (HIF1\u03b1) as not only a marker but also a driver of tendinopathy. Histological and multiomics evaluation of human tendinopathic samples revealed extensive extracellular matrix remodeling, including pathological collagen cross-linking coinciding with active hypoxic signaling. Hypothesizing a causal contribution of hypoxia signaling, we generated mice with tenocyte-targeted deletions of the von Hippel\u2013Lindau (\n                    <jats:italic toggle=\"yes\">Vhl<\/jats:italic>\n                    ) gene, which controls hypoxia signaling by regulating HIF\u03b1 degradation.\n                    <jats:italic toggle=\"yes\">Vhl<\/jats:italic>\n                    inactivation was sufficient to induce pathological hallmarks of tendinopathy, such as collagen matrix disorganization, cross-linking, altered mechanics, and neurovascular ingrowth. This phenotype was HIF1\u03b1 dependent given that codeleting HIF1\u03b1 rescued tendon morphology and mechanics. Moreover, deleting vascular endothelial growth factor A (\n                    <jats:italic toggle=\"yes\">Vegfa<\/jats:italic>\n                    ) alongside VHL effectively suppressed neovascularization but failed to rescue extracellular matrix abnormalities or restore mechanical function, emphasizing a direct role of HIF1\u03b1 in driving tendon disease independently of angiogenesis. Mechanistically, we found that HIF1\u03b1 activation was strain dependent in primary cultured human tendon cells and induced by mechanical overload in murine tendon explants. Furthermore, genetically removing\n                    <jats:italic toggle=\"yes\">Hif1<\/jats:italic>\n                    \u03b1 from tenocytes prevented aberrant tendon remodeling in response to chronic overload. These findings position HIF1\u03b1 signaling as a central driver of tendinopathy that acts through a maladaptive tissue response to chronic overload, providing mechanistic insights that could be leveraged for therapeutic approaches.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adt1228","type":"journal-article","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T18:58:20Z","timestamp":1767812300000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":10,"title":["HIF1\u03b1 gates tendon response to overload and drives tendinopathy independently of vascular recruitment"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9845-9965","authenticated-orcid":true,"given":"Greta","family":"Moschini","sequence":"first","affiliation":[{"name":"University Hospital Balgrist, University of Zurich, 8008 Zurich, Switzerland."},{"name":"Institute for Biomechanics, ETH Zurich, 8008 Zurich, Switzerland."},{"name":"Laboratory of Exercise and Health, ETH Zurich, 8603 Zurich, Switzerland."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-8109-0651","authenticated-orcid":true,"given":"Archana G.","family":"Mohanan","sequence":"additional","affiliation":[{"name":"Babraham Institute, Babraham Research Campus, CB22 3AT Cambridge, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1672-5033","authenticated-orcid":true,"given":"Izabella S.","family":"Niewczas","sequence":"additional","affiliation":[{"name":"Babraham Institute, Babraham Research Campus, CB22 3AT Cambridge, UK."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-4940-9352","authenticated-orcid":true,"given":"Diane E.","family":"Taylor","sequence":"additional","affiliation":[{"name":"Babraham Institute, Babraham Research Campus, CB22 3AT Cambridge, 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