{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14(1)"],"submitter":["Chen J"],"pubmed_abstract":["Ischemia reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The role of N<sup>6-</sup>methyladenosine (m6A) modification in AKI remains unclear. Here, we characterize the role of AlkB homolog 5 (ALKBH5) and m6A modification in an I/R-induced renal injury model in male mice. Alkbh5-knockout mice exhibit milder pathological damage and better renal function than wild-type mice post-IRI, whereas Alkbh5-knockin mice show contrary results. Also conditional knockout of Alkbh5 in the tubular epithelial cells alleviates I/R-induced AKI and fibrosis. CCL28 is identified as a target of ALKBH5. Furthermore, Ccl28 mRNA stability increases with Alkbh5 deficiency, mediating by the binding of insulin-like growth factor 2 binding protein 2. Treg recruitment is upregulated and inflamma"],"journal":["Nature communications"],"pagination":["1161"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9977869"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment."],"pmcid":["PMC9977869"],"pubmed_authors":["Gao R","Chen J","Yang K","Rong R","Cao Y","Xu C","Liang L","Xu S","Chen S","Wang J","Zhu T"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment.","description":"Ischemia reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The role of N<sup>6-</sup>methyladenosine (m6A) modification in AKI remains unclear. Here, we characterize the role of AlkB homolog 5 (ALKBH5) and m6A modification in an I/R-induced renal injury model in male mice. Alkbh5-knockout mice exhibit milder pathological damage and better renal function than wild-type mice post-IRI, whereas Alkbh5-knockin mice show contrary results. Also conditional knockout of Alkbh5 in the tubular epithelial cells alleviates I/R-induced AKI and fibrosis. CCL28 is identified as a target of ALKBH5. Furthermore, Ccl28 mRNA stability increases with Alkbh5 deficiency, mediating by the binding of insulin-like growth factor 2 binding protein 2. Treg recruitment is upregulated and inflamma","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-18T14:12:40.347Z","creation":"2025-04-07T00:13:07.514Z"},"accession":"S-EPMC9977869","cross_references":{"pubmed":["36859428"],"doi":["10.1038/s41467-023-36747-y"]}}