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This study was aimed at exploring the biological function and molecular mechanism of ferroptosis of LRP6 modulation in cardiomyocytes of myocardial infarction (MI). <jats:italic>Method<\/jats:italic>. We established the ferroptosis model of MI in vivo and in vitro and constructed the modulation network of circRNA\u2010miRNA\u2010LRP6 by bioinformatics analysis; then, we focused on exploring the regulatory relationship of LRP6 and its upstream genes circRNA1615 and miR\u2010152\u20103p in the RIP experiments and the double luciferase reporter gene assay. Also, we tested the LRP6\u2010mediated autophagy\u2010related ferroptosis in MI. <jats:italic>Results<\/jats:italic>. Ferroptosis was found in cardiomyocytes of MI, and ferroptosis inhibitor Ferrostatin\u20101 (Fer\u20101) could improve the pathological process of MI. LRP6 was involved in the process of ferroptosis in cardiomyocytes, and LRP6 deletion regulated ferroptosis in cardiomyocytes through autophagy. Screening and identification of the upstream gene circRNA1615 would target LRP6. circRNA1615 inhibited ferroptosis in cardiomyocytes, and circRNA1615 could regulate the expression of LRP6 through sponge adsorption of miR\u2010152\u20103p, prevent LRP6\u2010mediated autophagy\u2010related ferroptosis in cardiomyocytes, and finally control the pathological process of MI. <jats:italic>Conclusions<\/jats:italic>. circRNA1615 inhibits ferroptosis via modulation of autophagy by the miRNA152\u20103p\/LRP6 molecular axis in cardiomyocytes of myocardial infarction.<\/jats:p>","DOI":"10.1155\/2021\/8963987","type":"journal-article","created":{"date-parts":[[2021,10,20]],"date-time":"2021-10-20T18:06:59Z","timestamp":1634753219000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Effect and Mechanism of LRP6 on Cardiac Myocyte Ferroptosis in Myocardial 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