<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Li X</submitter><funding>National Natural Science Foundation of China</funding><pubmed_abstract>Incomplete recovery from acute kidney injury induced by folic acid is a major risk factor for progression to chronic kidney disease. Mitochondrial dysfunction has been considered a crucial contributor to maladaptive repair in acute kidney injury. Treatment with FG-4592, an inhibitor of hypoxia inducible factor prolyl-hydroxylase, is emerging as a new approach to attenuate renal damage; however, the underlying mechanism has not been fully elucidated. The current research demonstrated the protective effect of FG-4592 against renal dysfunction and histopathological damage on the 7th day after FA administration. FG-4592 accelerated tubular repair by promoting tubular cell regeneration, as indicated by increased proliferation of cell nuclear antigen-positive tubular cells, and facilitated struc</pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>788977</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8915431</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Roxadustat (FG-4592) Facilitates Recovery From Renal Damage by Ameliorating Mitochondrial Dysfunction Induced by Folic Acid.</pubmed_title><pmcid>PMC8915431</pmcid><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Zou Y</pubmed_authors><pubmed_authors>Fu YY</pubmed_authors><pubmed_authors>Zhai XY</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Jiang B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Roxadustat (FG-4592) Facilitates Recovery From Renal Damage by Ameliorating Mitochondrial Dysfunction Induced by Folic Acid.</name><description>Incomplete recovery from acute kidney injury induced by folic acid is a major risk factor for progression to chronic kidney disease. Mitochondrial dysfunction has been considered a crucial contributor to maladaptive repair in acute kidney injury. Treatment with FG-4592, an inhibitor of hypoxia inducible factor prolyl-hydroxylase, is emerging as a new approach to attenuate renal damage; however, the underlying mechanism has not been fully elucidated. The current research demonstrated the protective effect of FG-4592 against renal dysfunction and histopathological damage on the 7th day after FA administration. FG-4592 accelerated tubular repair by promoting tubular cell regeneration, as indicated by increased proliferation of cell nuclear antigen-positive tubular cells, and facilitated struc</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2025-08-23T03:08:57.482Z</modification><creation>2025-04-04T14:50:37.694Z</creation></dates><accession>S-EPMC8915431</accession><cross_references><pubmed>35280255</pubmed><doi>10.3389/fphar.2021.788977</doi></cross_references></HashMap>