<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hu M</submitter><funding>National Natural Science Foundation of China</funding><pagination>2023500</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9492344</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2022</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Acute lung injury (ALI) is a clinical disease with high morbidity and mortality, with limited treatment means. For primary alveolar epithelial type II (AT2) cells, glycolysis is an essential bioenergetic process. However, the significance of AT2 cell glycolysis in sepsis ALI remains unknown.&lt;h4>Methods and results&lt;/h4>In the current study, based on microarray analysis, real-time quantitative PCR, and Western blotting, we found that the hsa00020: citrate cycle pathway was inactivated, specifically its downstream gene: malate dehydrogenase 1 (MDH1) and MDH2 in ALI. In this context, lipopolysaccharides (LPS) were used to construct the septic-ALI mouse model and the biological function of MDH1 and MDH2 in primary alveolar epithelial type II (AT2) cells was explored. Through </pubmed_abstract><journal>Computational and mathematical methods in medicine</journal><pubmed_title>MDH1 and MDH2 Promote Cell Viability of Primary AT2 Cells by Increasing Glucose Uptake.</pubmed_title><pmcid>PMC9492344</pmcid><funding_grant_id>2019 81971869</funding_grant_id><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Hu M</pubmed_authors><pubmed_authors>Xu Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>MDH1 and MDH2 Promote Cell Viability of Primary AT2 Cells by Increasing Glucose Uptake.</name><description>&lt;h4>Background&lt;/h4>Acute lung injury (ALI) is a clinical disease with high morbidity and mortality, with limited treatment means. For primary alveolar epithelial type II (AT2) cells, glycolysis is an essential bioenergetic process. However, the significance of AT2 cell glycolysis in sepsis ALI remains unknown.&lt;h4>Methods and results&lt;/h4>In the current study, based on microarray analysis, real-time quantitative PCR, and Western blotting, we found that the hsa00020: citrate cycle pathway was inactivated, specifically its downstream gene: malate dehydrogenase 1 (MDH1) and MDH2 in ALI. In this context, lipopolysaccharides (LPS) were used to construct the septic-ALI mouse model and the biological function of MDH1 and MDH2 in primary alveolar epithelial type II (AT2) cells was explored. Through </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-06-04T12:26:56.716Z</modification><creation>2024-10-19T09:18:58.578Z</creation></dates><accession>S-EPMC9492344</accession><cross_references><pubmed>36158123</pubmed><doi>10.1155/2022/2023500</doi></cross_references></HashMap>