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- W3184005283 abstract "Abstract Background : The activated nuclear factor (NF)-κB pathway in atherosclerotic plaques promotes the progression of atherosclerosis. Targeting of plaque NF-κB may provide a novel strategy for limiting chronic inflammation. This study was conducted to examine the effect of NF-κB inhibition by using recombinant adeno-associated virus 9 (AAV9) to deliver IκBα (AAV9‐IκBα) which can be overexpressed to influence atherosclerosis. Methods and Results : Systemic delivery of AAV9‐IκBα resulted in ~2-fold overexpression of IκBα protein in the atherosclerotic plaques of apolipoprotein E -/- mice fed a high-fat diet. AAV9‐IκBα delivery did not affect the body weight or lipid deposition and plaque size in the mice. During plaque formation, overexpression of IκBα suppressed intra-plaque macrophage infiltration, inhibited the expression of pro-inflammatory genes including interleukin-6, monocyte chemoattractant protein-1, tumor necrosis factor-α and matrix metalloproteinase, enhanced the contents of collagen and vascular smooth muscle cells, and decreased the plaque vulnerability index by inhibiting the phosphorylation of NF-κB subunit p65 and its nuclear translocation. Conclusions : Systemic delivery of AAV9-IκBα promotes plaque stability by inhibiting NF-κB activation and suppressing intra-plaque inflammation, suggesting that inhibition of the NF-κB pathway in atherosclerotic plaques is a promising approach for treating atherosclerosis." @default.
- W3184005283 created "2021-08-02" @default.
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- W3184005283 date "2021-07-28" @default.
- W3184005283 modified "2023-10-16" @default.
- W3184005283 title "Systemic delivery of rAAV9‐IκBα stabilized atherosclerotic plaques and attenuated intra-plaque inflammation by inhibiting nuclear factor-κB activation in apolipoprotein E–deficient mice" @default.
- W3184005283 doi "https://doi.org/10.21203/rs.3.rs-748433/v1" @default.
- W3184005283 hasPublicationYear "2021" @default.
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