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Although genetically determined (e.g.,\n                    <jats:italic>PKP2<\/jats:italic>\n                    mutations), ACM phenotypes are highly variable. More data on phenotype modulators, clinical prognosticators, and etiological therapies are awaited. We hypothesized that oxidized low\u2010density lipoprotein (oxLDL)\u2010dependent activation of PPAR\u03b3, a recognized effector of ACM adipogenesis, contributes to disease pathogenesis. ACM patients showing high plasma concentration of oxLDL display severe clinical phenotypes in terms of fat infiltration, ventricular dysfunction, and major arrhythmic event risk. In ACM patient\u2010derived cardiac cells, we demonstrated that oxLDLs are major cofactors of adipogenesis. Mechanistically, the increased lipid accumulation is mediated by oxLDL cell internalization through CD36, ultimately resulting in PPAR\u03b3 upregulation. By boosting oxLDL in a\n                    <jats:italic>Pkp2<\/jats:italic>\n                    heterozygous knock\u2010out mice through high\u2010fat diet feeding, we confirmed\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    the oxidized lipid dependency of cardiac adipogenesis and right ventricle systolic impairment, which are counteracted by atorvastatin treatment. The modulatory role of oxidized lipids on ACM adipogenesis, demonstrated at cellular, mouse, and patient levels, represents a novel risk stratification tool and a target for ACM pharmacological strategies.\n                  <\/jats:p>","DOI":"10.15252\/emmm.202114365","type":"journal-article","created":{"date-parts":[[2021,8,2]],"date-time":"2021-08-02T03:27:34Z","timestamp":1627874854000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Oxidized LDL\u2010dependent pathway as new pathogenic trigger in arrhythmogenic 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