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Exogenous itaconate addition in apolipoprotein E-deficient (Apoe−/−) mice suppressed the initiation and progression of AAA and downstream inflammatory protein even though Irg1 deficiency reverted the result of inhibitory. Overexpression of Keap1 or transferred Cys151S mutant Keap1 vector also abolished the activation of Nrf2 induced by itaconat

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