{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T15:49:24Z","timestamp":1789746564258,"version":"4.0.1"},"reference-count":76,"publisher":"American Society for Clinical Investigation","issue":"5","license":[{"start":{"date-parts":[[2025,3,3]],"date-time":"2025-03-03T00:00:00Z","timestamp":1740960000000},"content-version":"vor","delay-in-days":48,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["R01AR042423,R01AR049899,T32AR007612,T32AG029796"],"award-info":[{"award-number":["R01AR042423,R01AR049899,T32AR007612,T32AG029796"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,3,3]]},"abstract":"<jats:p>\n                    Eccentric contraction\u2013induced (ECC-induced) force loss is a hallmark of murine dystrophin-deficient (\n                    <jats:italic>mdx<\/jats:italic>\n                    ) skeletal muscle that is used to assess efficacy of potential therapies for Duchenne muscular dystrophy. While virtually all key proteins involved in muscle contraction have been implicated in ECC force loss, a unifying mechanism that orchestrates force loss across such diverse molecular targets has not been identified. We showed that correcting defective hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) signaling in\n                    <jats:italic>mdx<\/jats:italic>\n                    muscle prevented ECC force loss. We also showed that the cysteine proteome of skeletal muscle functioned as a redox buffer in WT and\n                    <jats:italic>mdx<\/jats:italic>\n                    muscle during ECCs, but that buffer capacity in\n                    <jats:italic>mdx<\/jats:italic>\n                    muscle was significantly compromised by elevated basal protein oxidation. Finally, chemo-proteomic data suggested that H\n                    <jats:sub>2<\/jats:sub>\n                    S protected several proteins central to muscle contraction against irreversible oxidation through persulfidation-based priming. Our results support a unifying, redox-based mechanism of ECC force loss in\n                    <jats:italic>mdx<\/jats:italic>\n                    muscle.\n                  <\/jats:p>","DOI":"10.1172\/jci176942","type":"journal-article","created":{"date-parts":[[2025,1,14]],"date-time":"2025-01-14T12:00:29Z","timestamp":1736856029000},"source":"Crossref","is-referenced-by-count":3,"title":["Impaired hydrogen sulfide biosynthesis underlies eccentric contraction\u2013induced force loss in dystrophin-deficient skeletal muscle"],"prefix":"10.1172","volume":"135","author":[{"given":"W. 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