ArticleMolecular biology reports2025
Inhibition of ACSL6 ameliorates atherosclerosis by suppressing macrophage ferroptosis via the Nrf2 pathway.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtherosclerosis (AS) is a chronic arterial disease. Macrophage ferroptosis, a form of iron-dependent cell death, contributes significantly to plaque formation. Acyl-CoA synthetase long-chain family member 6 (ACSL6) is associated with ferroptosis, but its regulatory role in AS is currently unknown. This study aimed to investigate the function and mechanism of ACSL6 in AS.
methodsWe established an AS model by feeding apolipoprotein E-deficient (ApoE
resultsACSL6 expression levels were elevated in both in vitro and in vivo AS models. Expression levels of glutathione peroxidase 4 (GPX4) and Xap5 circadian timekeeper (xCT) were decreased in AS. Immunofluorescence (IF) confirmed infiltration of CD68-positive macrophages and reduced GPX4 expression in the aortas of AS mice. Nrf2 nuclear translocation was inhibited. Knockdown of ACSL6 reversed these changes, while co-treatment with the Nrf2 inhibitor ML385 blocked the protective effects of ACSL6 knockdown.
conclusionIn conclusion, our results demonstrate that ACSL6 inhibition ameliorates AS by suppressing macrophage ferroptosis, a process in which the activation of the Nrf2 pathway plays a pivotal role. Our findings uncover a novel regulatory axis and provide new insights for the treatment of AS.
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