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7,40 While the activation of ALOX12 exacerbates the liver inflammatory response and cell death by producing 12-HETE, which directly binds to GPR31 and induces subsequent MAPK signaling, 40 the increase in ALOX12 expression in cardiomyocytes promotes myocardial damage through 12-HETE-induced inflammation and, more importantly, by directly enhancing NEDD4-mediated TAK1 (transforming growth factor-activated kinase 1) degradation in an enzymatic activityindependent manner

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