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Notably, the PCSK9 inhibition, by either the gene manipulation or anti-PCSK9 monoclonal antibodies, has been found to significantly attenuate ROS-mediated oxidative damage in the in vitro cellular model [45, 46] and various animal models [47, 48]

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1 Introduction In the United States, the prevalence of type 2 diabetes (T2D) has more than doubled in recent decades, affecting 12% of the population in 2025, while nearly two million individuals live with type 1 diabetes (T1D) ( SOD ), catalase ( CAT ), and the thioredoxin- and the glutathione-based systems, all regulated by the master OS regulator Nuclear Factor Erythroid 2-Related Factor 2 ( NRF2 ) ( High ROS levels induce irreversible damage to macromolecules by causing DNA strand breaks, lipid peroxidation (discussed further), and disruption of protein structure, stability and function ( 2 Biochemical mechanisms and detection methods of protein carbonylation Upon accumulation, ROS readily attack polyunsaturated -3 and -6 fatty acids (PUFAs) in membrane phospholipids through a well-established three-step process known as lipid peroxidation

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