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Here, we show that suppression of mitochondrial calcium uniporter (MCU)\u2010mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx into mitochondria in the body wall muscles of the nematode\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    improved the sarcopenic phenotypes, blunting movement and mitochondrial structural and functional decline with age. We found that normally aged muscle cells exhibited elevated resting mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    levels and increased mitophagy to eliminate damaged mitochondria. Similar to aging muscle, we found that suppressing MCU function in muscular dystrophy improved movement via reducing elevated resting mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    levels. 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Further, modulation of MCU activity may act as a potential pharmacological target in various conditions involving muscle loss.\n                  <\/jats:p>","DOI":"10.1096\/fj.202201489rr","type":"journal-article","created":{"date-parts":[[2023,3,19]],"date-time":"2023-03-19T22:00:07Z","timestamp":1679263207000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Increased mitochondrial Ca\n                    <sup>2+<\/sup>\n                    contributes to health decline with age and Duchene muscular dystrophy in\n                    <i>C. elegans<\/i>"],"prefix":"10.1096","volume":"37","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6920-0594","authenticated-orcid":false,"given":"Atsushi","family":"Higashitani","sequence":"first","affiliation":[{"name":"Graduate School of Life Sciences Tohoku University  Sendai 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