{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shi M"],"funding":["NIDDK NIH HHS"],"pagination":["63-78"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8741729"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["101(1)"],"pubmed_abstract":["Autophagy regulator beclin 1 activity determines the severity of kidney damage induced by ischemia reperfusion injury, but its role in kidney recovery and fibrosis are unknown and its therapeutic potentials have not been tested. Here, we explored beclin 1 effects on kidney fibrosis in three models of acute kidney injury (AKI)-ischemia reperfusion injury, cisplatin kidney toxicity, and unilateral ureteric obstruction in mouse strains with three levels of beclin 1 function: normal (wild type), low (heterozygous global deletion of beclin 1, Becn1<sup>+/-</sup>), and high beclin 1 activity (knockin gain-of-function mutant Becn1, Becn1<sup>FA</sup>). Fourteen days after AKI induction, heterozygous mice had more, but knockin mice had less kidney fibrosis than wild-type mice did. One day after is"],"journal":["Kidney international"],"pubmed_title":["In vivo evidence for therapeutic applications of beclin 1 to promote recovery and inhibit fibrosis after acute kidney injury."],"pmcid":["PMC8741729"],"funding_grant_id":["R01 DK092461","R01 DK091392","P30 DK079328"],"pubmed_authors":["Shi M","Maique J","Hu MC","Li P","Seli O","Moe OW","Shepard S"],"additional_accession":[]},"is_claimable":false,"name":"In vivo evidence for therapeutic applications of beclin 1 to promote recovery and inhibit fibrosis after acute kidney injury.","description":"Autophagy regulator beclin 1 activity determines the severity of kidney damage induced by ischemia reperfusion injury, but its role in kidney recovery and fibrosis are unknown and its therapeutic potentials have not been tested. Here, we explored beclin 1 effects on kidney fibrosis in three models of acute kidney injury (AKI)-ischemia reperfusion injury, cisplatin kidney toxicity, and unilateral ureteric obstruction in mouse strains with three levels of beclin 1 function: normal (wild type), low (heterozygous global deletion of beclin 1, Becn1<sup>+/-</sup>), and high beclin 1 activity (knockin gain-of-function mutant Becn1, Becn1<sup>FA</sup>). Fourteen days after AKI induction, heterozygous mice had more, but knockin mice had less kidney fibrosis than wild-type mice did. One day after is","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-19T18:08:15.31Z","creation":"2025-04-19T18:08:15.31Z"},"accession":"S-EPMC8741729","cross_references":{"pubmed":["34736972"],"doi":["10.1016/j.kint.2021.09.030"]}}