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This metabolic stress leads to defective insulin secretion, apoptosis, and dedifferentiation of β-cells owing to molecular causes involving a combination of mitochondrial dysfunction, autophagy impairment, inflammation, ER, and oxidative stress (Lytrivi et al., 2020)
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As all these are essential stages in the initiation and perpetuation of psoriasis, the hypothesis that oxidative stress plays a key role in the pathophysiology of this chronic dermatosis has emerged [10]
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