<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yu Y</submitter><funding>National Natural Science Foundation of China</funding><pagination>1907-1922</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525958</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(18)</volume><pubmed_abstract>Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. &lt;i>In vitro&lt;/i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, auto</pubmed_abstract><journal>Cell cycle (Georgetown, Tex.)</journal><pubmed_title>Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway.</pubmed_title><pmcid>PMC8525958</pmcid><funding_grant_id>Grant Number 81970659</funding_grant_id><funding_grant_id>Grant Number 81700664</funding_grant_id><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Qiao H</pubmed_authors><pubmed_authors>Shan Z</pubmed_authors><pubmed_authors>Wu D</pubmed_authors><pubmed_authors>Yu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway.</name><description>Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. &lt;i>In vitro&lt;/i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, auto</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2025-04-05T14:05:18.799Z</modification><creation>2025-04-05T14:05:18.799Z</creation></dates><accession>S-EPMC8525958</accession><cross_references><pubmed>34427546</pubmed><doi>10.1080/15384101.2021.1966199</doi></cross_references></HashMap>