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Specifically, treatment with quisinostat inhibits the expression of HDAC11 and reduces the interaction between HDAC11 and activator protein 2 (AP-2) on the KLF15 promoter to promote KLF15 transcription and upregulate KLF15 expression, thereby relieving renal fibrosis induced by UUO and Ang II (Mao et al., 2020) 5 Conclusion and perspectives Acetylation modification is a key PTM that is dynamically regulated by HATs and HDACs

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The effects of the KD on mitochondrial function may be from improving ATP energy metabolism, likely improving neuronal homeostasis and also enabling higher resilience to neural damage during seizures [57]

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