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To further elucidate the relationship between copper transporters and cardiac copper efflux during chronic myocardial ischemia, a rhesus monkey model was established by performing the permanent ligation of the left anterior descending coronary artery. A dramatic decrease in copper concentration within ischemic cardiomyocytes was observed alongside declining cardiac function. Among major copper transporters, COMMD1 and ATP7B were significantly upregulated in the ischemic myocardium. COMMD1 was specifically localised in cardiomyocytes undergoing copper efflux, whereas increased ATP7B was restricted to cardiac fibroblasts. This indicates that elevated COMMD1 regulates copper efflux in cardiomyocytes during chronic myocardial ischemia, functioning independently of its interactions with P\u2010type ATPase transporters. Given the discrepancy between RNA and protein levels of COMMD1 in ischemic myocardium, post\u2010translational modification is likely responsible for regulating COMMD1 expression. We found that the copper\u2010binding protein with E3 ubiquitin ligase activity, XIAP, augmented before the rise in COMMD1 expression within ischemic cardiomyocytes. Excessive XIAP specifically interacted with COMMD1 to enhance its protein levels under copper\u2010deprivation conditions and vice versa. Overall, our findings reveal a positive feedback loop among XIAP, COMMD1 and copper, highlighting the intricate interplay between XIAP and COMMD1 in regulating copper efflux in cardiomyocytes. This loop sets the stage for further investigation into therapeutic strategies to manage copper homeostasis in chronic myocardial ischemia.<\/jats:p>","DOI":"10.1111\/cpr.70016","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T19:48:13Z","timestamp":1741722493000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Elevated <scp>COMMD1<\/scp> Contributes to Cardiomyocyte Copper Efflux in Chronic Myocardial Ischemia: Insights From Rhesus Monkey"],"prefix":"10.1111","volume":"58","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4546-500X","authenticated-orcid":false,"given":"Chen","family":"Li","sequence":"first","affiliation":[{"name":"Department of Experimental Research, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital &amp; Institute, Sichuan Cancer Center University of Electronic Science and Technology of China  Chengdu Sichuan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Da","family":"Li","sequence":"additional","affiliation":[{"name":"Department of General Internal Medicine, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital &amp; 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