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These findings, in line with several recent studies reporting the protective effects of statins in various kidney diseases [42,43,44,45], underscore the critical role of lipid metabolic dysregulation in CaOx-induced renal injury and suggest that pharmacological modulation of lipid metabolism may serve as a complementary strategy to targeting the PRMT1/UBE2m axis

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Importantly, primary human ILC2s exhibited conserved NRF2 activation, glutathione accumulation, and reduced type 2 cytokine production in response to melatonin, underscoring clinical relevance