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The products of oxidized lipids, especially those derived from the PUFAs in lipid membranes that are attacked by reactive oxygen species (ROS) and reactive nitrogen species (RNS) are the ones that produce harm ( However, while excessive peroxidation of lipids is implicated in the pathogenesis of myriads of diseases, the same peroxidation of lipids provides the necessary signalling molecules for the regulation of very important cellular functions that incorporate the balance and regulation of autophagy (Zheng et al., 2024)

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Multiple mechanisms drive pathological ROS accumulation in diabetic cardiomyocytes, such as inhibition of mitochondrial oxidative phosphorylation elevating O 2 production, activation of NOX by angiotensin II (Ang II) and TNF-, and AGEs-RAGE binding-induced NF-B activation that triggers inflammation and further ROS generation