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Chemokine-mediated inflammatory cell infiltration and local inflammatory damage response are recent research hotspots. Hence, we attempted to examine the role of <jats:italic>C-X-C motif chemokine 16<\/jats:italic> (<jats:italic>CXCL16<\/jats:italic>) as a potential candidate in MI.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Human cardiomyocytes were treated with hypoxia\/reoxygenation (H\/R) to establish an in vitro cell model. GEO database provided the clinical data of MI patients and GSEA verified the relationship of chemokine and MI. CCK-8 and flow cytometry analyses were used to measure cell viability and apoptosis. Bioinformatics analysis and luciferase reporter assay were conducted to determine the correlation between <jats:italic>CXCL16<\/jats:italic> and <jats:italic>miR-545<\/jats:italic>. qRT-PCR and western blot assays were performed to investigate the expression level of the indicated genes. The activity of lactate dehydrogenase (LDH) and the levels of TNF-\u03b1, IL-6, IL-1\u03b2, and IL-10 were explored using ELISA assay.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>CXCL16 was increased in MI. CXCL16 knockdown can reverse the inhibitory effect of H\/R treatment on cell viability, while overexpression of CXCL16 showed the opposite trend. <jats:italic>MiR-545<\/jats:italic> directly targeted <jats:italic>CXCL16<\/jats:italic> and negatively regulated CXCL16 levels. <jats:italic>MiR-545<\/jats:italic> promoted cell proliferation and inhibited apoptosis in the MI cell model, which attenuated the CXCL16-induced injury on cardiomyocytes.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>These findings demonstrated that <jats:italic>CXCL16<\/jats:italic> aggravated MI damage through being directly targeted by <jats:italic>miR-545<\/jats:italic> and mediating inflammatory responses, thereby providing potential therapeutic targets for MI therapy.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s40246-021-00314-7","type":"journal-article","created":{"date-parts":[[2021,2,26]],"date-time":"2021-02-26T10:08:40Z","timestamp":1614334120000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["C-X-C motif chemokine 16, modulated by microRNA-545, aggravates myocardial damage and affects the inflammatory responses in myocardial infarction"],"prefix":"10.1186","volume":"15","author":[{"given":"Fang-Qian","family":"Liang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing-Yuan","family":"Gao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4402-7331","authenticated-orcid":false,"given":"Ji-Wei","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2021,2,26]]},"reference":[{"issue":"1","key":"314_CR1","doi-asserted-by":"publisher","first-page":"186","DOI":"10.1159\/000495173","volume":"51","author":"F He","year":"2018","unstructured":"He F, et al. 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