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Our previous work showed that E1 subunit phosphorylation makes a minor contribution to PDHC inhibition in activated macrophages 11 , likely explaining the small portion of PDHC inhibition that cannot be fully recovered by iNOS knockout

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In cellular and animal models of steroid insensitivity mediated by oxidative stress, S-CMC restored steroid sensitivity by increasing HDAC-2 expression/activity through elevating GSH and SOD levels, reducing oxidative stress, enhancing HDAC-2 recruitment and reducing H4 acetylation in the IL-8 promoter region, and eventually alleviating inflammation and lung damage [88, 89]