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Since LOX‐1, a key receptor involved in ox‐LDL phagocytosis and degradation in VECs, plays a significant role in atherosclerosis development, its silencing has been shown to inhibit OA‐induced Nrf2 and HO‐1 expression, indicating that LOX‐1 is involved in OA's protective effects on ECs (Jiang et al
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Endogenous FA has been suggested as a causative agent for the DNA repair-deficient condition Fanconi Anaemia 8,9,10
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