{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T20:24:44Z","timestamp":1792095884426,"version":"4.4.0"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"14","license":[{"start":{"date-parts":[[2023,7,31]],"date-time":"2023-07-31T00:00:00Z","timestamp":1690761600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL132899"],"award-info":[{"award-number":["R01 HL132899"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL147954"],"award-info":[{"award-number":["R01 HL147954"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL164584"],"award-info":[{"award-number":["R01 HL164584"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Aab Cardiovascular Research Institute of the University of Rochester Medical Center"},{"name":"American Heart Association Postdoctoral Fellowship","award":["19POST34400013"],"award-info":[{"award-number":["19POST34400013"]}]},{"name":"Career Development Award","award":["848985"],"award-info":[{"award-number":["848985"]}]},{"name":"NIH T32 Fellowship","award":["T32 GM068411"],"award-info":[{"award-number":["T32 GM068411"]}]},{"name":"NIH T32 Fellowship","award":["R01 HL154318"],"award-info":[{"award-number":["R01 HL154318"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>Mitochondria play a vital role in cellular metabolism and energetics and support normal cardiac function. Disrupted mitochondrial function and homeostasis cause a variety of heart diseases. Fam210a (family with sequence similarity 210 member A), a novel mitochondrial gene, is identified as a hub gene in mouse cardiac remodelling by multi-omics studies. Human FAM210A mutations are associated with sarcopenia. However, the physiological role and molecular function of FAM210A remain elusive in the heart. We aim to determine the biological role and molecular mechanism of FAM210A in regulating mitochondrial function and cardiac health in vivo.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Tamoxifen-induced \u03b1MHCMCM-driven conditional knockout of Fam210a in the mouse cardiomyocytes induced progressive dilated cardiomyopathy and heart failure, ultimately causing mortality. Fam210a deficient cardiomyocytes exhibit severe mitochondrial morphological disruption and functional decline accompanied by myofilament disarray at the late stage of cardiomyopathy. Furthermore, we observed increased mitochondrial reactive oxygen species production, disturbed mitochondrial membrane potential, and reduced respiratory activity in cardiomyocytes at the early stage before contractile dysfunction and heart failure. Multi-omics analyses indicate that FAM210A deficiency persistently activates integrated stress response, resulting in transcriptomic, translatomic, proteomic, and metabolomic reprogramming, ultimately leading to pathogenic progression of heart failure. Mechanistically, mitochondrial polysome profiling analysis shows that FAM210A loss of function compromises mitochondrial mRNA translation and leads to reduced mitochondrial-encoded proteins, followed by disrupted proteostasis. We observed decreased FAM210A protein expression in human ischaemic heart failure and mouse myocardial infarction tissue samples. To further corroborate FAM210A function in the heart, AAV9-mediated overexpression of FAM210A promotes mitochondrial-encoded protein expression, improves cardiac mitochondrial function, and partially rescues murine hearts from cardiac remodelling and damage in ischaemia-induced heart failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results suggest that FAM210A is a mitochondrial translation regulator to maintain mitochondrial homeostasis and normal cardiomyocyte contractile function. This study also offers a new therapeutic target for treating ischaemic heart disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvad124","type":"journal-article","created":{"date-parts":[[2023,7,29]],"date-time":"2023-07-29T08:48:10Z","timestamp":1690620490000},"page":"2441-2457","source":"Crossref","is-referenced-by-count":15,"title":["FAM210A regulates mitochondrial translation and maintains cardiac mitochondrial homeostasis"],"prefix":"10.1093","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3109-417X","authenticated-orcid":false,"given":"Jiangbin","family":"Wu","sequence":"first","affiliation":[{"name":"Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine & Dentistry , 601 Elmwood Avenue, Rochester, NY 14642 , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kadiam C Venkata","family":"Subbaiah","sequence":"additional","affiliation":[{"name":"Aab Cardiovascular Research 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