{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T20:14:53Z","timestamp":1784578493167,"version":"3.55.0"},"reference-count":36,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2019,5,29]],"date-time":"2019-05-29T00:00:00Z","timestamp":1559088000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81570306"],"award-info":[{"award-number":["81570306"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Myeloid differentiation 1 (MD\u20101) is a secreted protein that regulates the immune response of B cell through interacting with radioprotective 105 (RP105). Disrupted immune response may contribute to the development of cardiac diseases, while the roles of MD\u20101 remain elusive. Our studies aimed to explore the functions and molecular mechanisms of MD\u20101 in obesity\u2010induced cardiomyopathy. H9C2 myocardial cells were treated with free fatty acid (FFA) containing palmitic acid and oleic acid to challenge high\u2010fat stimulation and adenoviruses harbouring human MD\u20101 coding sequences or shRNA for MD\u20101 overexpression or knockdown in vitro. MD\u20101 overexpression or knockdown transgenic mice were generated to assess the effects of MD\u20101 on high\u2010fat diet (HD) induced cardiomyopathy in vivo. Our results showed that MD\u20101 was down\u2010regulated in H9C2 cells exposed to FFA stimulation for 48\u00a0hours and in obesity mice induced by HD for 20\u00a0weeks. Both in vivo and in vitro<jats:italic>,<\/jats:italic> silencing of MD\u20101 accelerated myocardial function injury induced by HD stimulation through increased cardiac hypertrophy and fibrosis, while overexpression of MD\u20101 alleviated the effects of HD by inhibiting the process of cardiac remodelling. Moreover, the MAPK and NF\u2010\u03baB pathways were overactivated in MD\u20101 deficient mice and H9C2 cells after high\u2010fat treatment. Inhibition of MAPK and NF\u2010\u03baB pathways played a cardioprotective role against the adverse effects of MD\u20101 silencing on high\u2010fat stimulation induced pathological remodelling. In conclusion, MD\u20101 protected myocardial function against high\u2010fat stimulation induced cardiac pathological remodelling through negative regulation for MAPK\/NF\u2010\u03baB signalling pathways, providing feasible strategies for obesity cardiomyopathy.<\/jats:p>","DOI":"10.1111\/jcmm.14407","type":"journal-article","created":{"date-parts":[[2019,5,29]],"date-time":"2019-05-29T11:45:53Z","timestamp":1559130353000},"page":"5303-5316","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Myeloid differentiation protein 1 protected myocardial function against high\u2010fat stimulation induced pathological remodelling"],"prefix":"10.1111","volume":"23","author":[{"given":"Cai\u2010Jie","family":"Shen","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan PR China"},{"name":"Cardiovascular Research Institute of Wuhan University Wuhan PR China"},{"name":"Hubei 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