{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wei Q"],"funding":["BLRD VA","National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","National Natural Science Foundation of China","US Department of Veterans Affairs"],"pagination":["249-262"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11764320"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["33(1)"],"pubmed_abstract":["Epigenetic regulations, such as DNA methylation and microRNAs, play an important role in renal fibrosis. Here, we report the regulation of microRNA219a-2 by DNA methylation in fibrotic kidneys, unveiling the crosstalk between these epigenetic mechanisms. Through genome-wide DNA methylation analysis and pyrosequencing, we detected the hypermethylation of microRNA219a-2 in renal fibrosis induced by unilateral ureteral obstruction (UUO) or renal ischemia/reperfusion, which was accompanied by a significant decrease in microRNA-219a-5p expression. Functionally, overexpression of microRNA219a-2 enhanced fibronectin induction during hypoxia or TGF-β1 treatment of cultured renal cells. In mice, inhibition of microRNA-219a-5p suppressed fibronectin accumulation in UUO and ischemic/reperfused kidney"],"journal":["Molecular therapy : the journal of the American Society of Gene Therapy"],"pubmed_title":["Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis."],"pmcid":["PMC11764320"],"funding_grant_id":["R01 DK058831","R01 DK087843","I01 BX000319","R01 DK126763","IK6 BX005236"],"pubmed_authors":["Wei Q","Hu X","Dong Z","Xiao X","Huo E","Guo C","Zhou X","Dong C","Shi H"],"additional_accession":[]},"is_claimable":false,"name":"Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.","description":"Epigenetic regulations, such as DNA methylation and microRNAs, play an important role in renal fibrosis. Here, we report the regulation of microRNA219a-2 by DNA methylation in fibrotic kidneys, unveiling the crosstalk between these epigenetic mechanisms. Through genome-wide DNA methylation analysis and pyrosequencing, we detected the hypermethylation of microRNA219a-2 in renal fibrosis induced by unilateral ureteral obstruction (UUO) or renal ischemia/reperfusion, which was accompanied by a significant decrease in microRNA-219a-5p expression. Functionally, overexpression of microRNA219a-2 enhanced fibronectin induction during hypoxia or TGF-β1 treatment of cultured renal cells. In mice, inhibition of microRNA-219a-5p suppressed fibronectin accumulation in UUO and ischemic/reperfused kidney","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-06T19:34:14.458Z","creation":"2026-06-04T03:10:51.278Z"},"accession":"S-EPMC11764320","cross_references":{"pubmed":["39295147"],"doi":["10.1016/j.ymthe.2024.09.020"]}}