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A recent study has described the pathological mechanism by which histone crotonylation modification regulates renal fibrosis, and proposed a potential therapeutic strategy: by inhibiting the activity of ACSS2 and reducing histone crotonylation, thereby affecting the IL-1β-mediated activation of macrophages and the aging process of renal tubular cells, in order to achieve the goal of alleviating renal fibrosis (Li et al., 2024)
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