YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RIP-Seq]
The pathogenesis of acute kidney injury (AKI), a serious complication with no effective therapy available, is complex and multifactorial. Here we show that renal tubular m6A reader YTHDF1 mitigates AKI through selectively recruiting m6A-modified mRNAs, many of which are essential for cell proliferation and survival, into stress granules (SGs) and safeguarding these methylated mRNAs in SGs until stress relief. This study provides YTHDF1, as well as its associated m6A mRNAs and SGs, as novel therapeutic targets for AKI treatment. Overall design: Detect genes that binding with YTHDF1 in human renal tubular epithelial cells(HK2 cells)