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39 The cellular levels of free ferrous iron were increased by the excessive formation of NADH through the metabolism of allyl alcohol by alcohol dehydrogenase and acrolein by aldehyde dehydrogenase

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Experimental results demonstrated that apelin-13, an endogenous ligand of the G protein-coupled receptor angiotensin II protein J (APJ), increased DRP1 expression, inhibited fusion-related protein expression, and stimulated VSMC mitophagy and abnormal proliferation, which exacerbated the development of atherosclerosis [227]

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