{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T02:29:41Z","timestamp":1788834581420,"version":"build-2803163510"},"reference-count":59,"publisher":"American Society for Clinical Investigation","issue":"9","license":[{"start":{"date-parts":[[2024,5,8]],"date-time":"2024-05-08T00:00:00Z","timestamp":1715126400000},"content-version":"vor","delay-in-days":36,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"crossref","award":["AR069107"],"award-info":[{"award-number":["AR069107"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"crossref","award":["R01HL133294,R01HL157116"],"award-info":[{"award-number":["R01HL133294,R01HL157116"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"crossref","award":["18IPA3417002"],"award-info":[{"award-number":["18IPA3417002"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,5,8]]},"abstract":"<jats:p>\n                    Duchenne muscular dystrophy (DMD) is a progressive muscle-wasting disease associated with cardiomyopathy. DMD cardiomyopathy is characterized by abnormal intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis and mitochondrial dysfunction. We used dystrophin and utrophin double-knockout (\n                    <jats:italic>\n                      mdx:utrn\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    ) mice in a sarcolipin (SLN) heterozygous-knockout (\n                    <jats:italic>\n                      sln\n                      <jats:sup>+\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    ) background to examine the effect of SLN reduction on mitochondrial function in the dystrophic myocardium. Germline reduction of SLN expression in\n                    <jats:italic>\n                      mdx:utrn\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice improved cardiac sarco\/endoplasmic reticulum (SR) Ca\n                    <jats:sup>2+<\/jats:sup>\n                    cycling, reduced cardiac fibrosis, and improved cardiac function. At the cellular level, reducing SLN expression prevented mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    overload, reduced mitochondrial membrane potential loss, and improved mitochondrial function. Transmission electron microscopy of myocardial tissues and proteomic analysis of mitochondria-associated membranes showed that reducing SLN expression improved mitochondrial structure and SR-mitochondria interactions in dystrophic cardiomyocytes. These findings indicate that SLN upregulation plays a substantial role in the pathogenesis of cardiomyopathy and that reducing SLN expression has clinical implications in the treatment of DMD cardiomyopathy.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.170185","type":"journal-article","created":{"date-parts":[[2024,4,2]],"date-time":"2024-04-02T12:01:31Z","timestamp":1712059291000},"source":"Crossref","is-referenced-by-count":8,"title":["Improved mitochondrial function in the hearts of sarcolipin-deficient dystrophin and utrophin double-knockout mice"],"prefix":"10.1172","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7804-9088","authenticated-orcid":true,"given":"Satvik","family":"Mareedu","sequence":"first","affiliation":[{"name":"Department of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers University, Newark, New Jersey, 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