<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lin HY</submitter><funding>Ministry of Science and Technology, Taiwan</funding><funding>Kaohsiung Municipal Ta-Tung Hospital</funding><pagination>620-634</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11055741</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(5-6)</volume><pubmed_abstract>Maleic acid (MA) induces renal tubular cell dysfunction directed to acute kidney injury (AKI). AKI is an increasing global health burden due to its association with mortality and morbidity. However, targeted therapy for AKI is lacking. Previously, we determined mitochondrial-associated proteins are MA-induced AKI affinity proteins. We hypothesized that mitochondrial dysfunction in tubular epithelial cells plays a critical role in AKI. In vivo and in vitro systems have been used to test this hypothesis. For the in vivo model, C57BL/6 mice were intraperitoneally injected with 400 mg/kg body weight MA. For the in vitro model, HK-2 human proximal tubular epithelial cells were treated with 2 mM or 5 mM MA for 24 h. AKI can be induced by administration of MA. In the mice injected with MA, the le</pubmed_abstract><journal>Apoptosis : an international journal on programmed cell death</journal><pubmed_title>Critical roles of tubular mitochondrial ATP synthase dysfunction in maleic acid-induced acute kidney injury.</pubmed_title><pmcid>PMC11055741</pmcid><funding_grant_id>109-2314-B-037-094</funding_grant_id><funding_grant_id>kmtth-109-R008</funding_grant_id><funding_grant_id>kmtth-108-007</funding_grant_id><funding_grant_id>kmtth-105-054</funding_grant_id><funding_grant_id>110-2314-B-037-068-MY3</funding_grant_id><pubmed_authors>Lin HC</pubmed_authors><pubmed_authors>Liang CJ</pubmed_authors><pubmed_authors>Yang MY</pubmed_authors><pubmed_authors>Chen PL</pubmed_authors><pubmed_authors>Lin CS</pubmed_authors><pubmed_authors>Wang TM</pubmed_authors><pubmed_authors>Chiang CK</pubmed_authors><pubmed_authors>Chiu CC</pubmed_authors><pubmed_authors>Lin HY</pubmed_authors><pubmed_authors>Chen YH</pubmed_authors><pubmed_authors>Shih YH</pubmed_authors><pubmed_authors>Liu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Critical roles of tubular mitochondrial ATP synthase dysfunction in maleic acid-induced acute kidney injury.</name><description>Maleic acid (MA) induces renal tubular cell dysfunction directed to acute kidney injury (AKI). AKI is an increasing global health burden due to its association with mortality and morbidity. However, targeted therapy for AKI is lacking. Previously, we determined mitochondrial-associated proteins are MA-induced AKI affinity proteins. We hypothesized that mitochondrial dysfunction in tubular epithelial cells plays a critical role in AKI. In vivo and in vitro systems have been used to test this hypothesis. For the in vivo model, C57BL/6 mice were intraperitoneally injected with 400 mg/kg body weight MA. For the in vitro model, HK-2 human proximal tubular epithelial cells were treated with 2 mM or 5 mM MA for 24 h. AKI can be induced by administration of MA. In the mice injected with MA, the le</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2026-05-29T09:44:17.6Z</modification><creation>2025-07-27T03:11:05.957Z</creation></dates><accession>S-EPMC11055741</accession><cross_references><pubmed>38281282</pubmed><doi>10.1007/s10495-023-01897-3</doi></cross_references></HashMap>