In acute kidney injury (AKI), dysregulated tissue regeneration can promote fibrosis and chronic kidney disease. Sustained SOX9 expression after AKI is a key promoter of fibrosis, according to a new study by Sanjeev Kumar and colleagues.

Epigenetic analyses suggest that cells with persistent SOX9 expression have a progenitor cell-like phenotype with patterns of chromatin reorganization that are associated with nephrogenesis and are distinct from those of SOX9^– cells.

中文翻译：

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AKI 后关闭 SOX9 以促进上皮细胞恢复

在急性肾损伤（AKI）中，组织再生失调会促进纤维化和慢性肾脏疾病。 Sanjeev Kumar 及其同事的一项新研究表明，AKI 后 SOX9 的持续表达是纤维化的关键促进因素。

表观遗传学分析表明，持续表达 SOX9 的细胞具有祖细胞样表型，其染色质重组模式与肾发生相关，并且与 SOX9^细胞不同。