<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tian Y</submitter><funding>Key Discipline Construction Project of Shanghai Pudong New Area Health Commission</funding><funding>Small and Micro Science and Technology Project of National Health Commission</funding><pagination>751</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12289799</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>52(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Nephrotoxicity is a common adverse effect of many chemotherapeutic agents and represents a major dose-limiting factor in cancer treatment. Therefore, developing effective renoprotective strategies is urgently needed. Molecular hydrogen (H&lt;sub>2&lt;/sub>) has emerged as a therapeutic agent with potent antioxidant and anti-inflammatory properties, selectively scavenging hydroxyl radicals and alleviating tissue injury. However, the protective effects and underlying mechanisms of H&lt;sub>2&lt;/sub> in chemotherapy-induced acute kidney injury (AKI) remain poorly understood.&lt;h4>Methods&lt;/h4>A cisplatin-induced AKI mouse model was established with or without H₂ administration. Kidney injury biomarkers were evaluated, and levels of inflammation and apoptosis were assessed using TUNEL sta</pubmed_abstract><journal>Molecular biology reports</journal><pubmed_title>Molecular hydrogen attenuates cisplatin-induced nephrotoxicity by modulating β-hydroxybutyrate metabolism.</pubmed_title><pmcid>PMC12289799</pmcid><funding_grant_id>20004</funding_grant_id><funding_grant_id>PWZxk2022-20</funding_grant_id><pubmed_authors>Fan W</pubmed_authors><pubmed_authors>Geng X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Tian Y</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Tang W</pubmed_authors><pubmed_authors>Su H</pubmed_authors><pubmed_authors>Wei Y</pubmed_authors><pubmed_authors>Zhou J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Molecular hydrogen attenuates cisplatin-induced nephrotoxicity by modulating β-hydroxybutyrate metabolism.</name><description>&lt;h4>Background&lt;/h4>Nephrotoxicity is a common adverse effect of many chemotherapeutic agents and represents a major dose-limiting factor in cancer treatment. Therefore, developing effective renoprotective strategies is urgently needed. Molecular hydrogen (H&lt;sub>2&lt;/sub>) has emerged as a therapeutic agent with potent antioxidant and anti-inflammatory properties, selectively scavenging hydroxyl radicals and alleviating tissue injury. However, the protective effects and underlying mechanisms of H&lt;sub>2&lt;/sub> in chemotherapy-induced acute kidney injury (AKI) remain poorly understood.&lt;h4>Methods&lt;/h4>A cisplatin-induced AKI mouse model was established with or without H₂ administration. Kidney injury biomarkers were evaluated, and levels of inflammation and apoptosis were assessed using TUNEL sta</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jul</publication><modification>2026-03-15T16:16:44.347Z</modification><creation>2025-08-13T03:04:42.539Z</creation></dates><accession>S-EPMC12289799</accession><cross_references><pubmed>40705191</pubmed><doi>10.1007/s11033-025-10845-0</doi></cross_references></HashMap>