<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>38(1)</volume><submitter>Wang L</submitter><pubmed_abstract>Sepsis is characterized by a severe inflammatory response throughout the whole body and can induce acute kidney injury (AKI). This research aimed to investigate the regulatory mechanisms underlying miR-155-5p in sepsis-induced AKI. CLP-treated mice were used as an in vivo model of sepsis-induced AKI, and LPS-treated HK-2 and TCMK-1 cells were used as in vitro models. Bioinformatics analyses and mechanistic assays were utilized to reveal the relationships between molecules. H&amp;E staining was used to reveal morphological changes in kidney tissues. ELISAs were conducted to detect the concentrations of proinflammatory cytokines. We discovered that miR-155-5p was prominently upregulated in sepsis-induced AKI in vivo and in vitro. MiR-155-5p inhibition alleviated kidney injury in mice. Moreover, </pubmed_abstract><journal>The Kaohsiung journal of medical sciences</journal><pagination>6-17</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11896158</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Long non-coding RNA XIST alleviates sepsis-induced acute kidney injury through inhibiting inflammation and cell apoptosis via regulating miR-155-5p/WWC1 axis.</pubmed_title><pmcid>PMC11896158</pmcid><pubmed_authors>Cao QM</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Long non-coding RNA XIST alleviates sepsis-induced acute kidney injury through inhibiting inflammation and cell apoptosis via regulating miR-155-5p/WWC1 axis.</name><description>Sepsis is characterized by a severe inflammatory response throughout the whole body and can induce acute kidney injury (AKI). This research aimed to investigate the regulatory mechanisms underlying miR-155-5p in sepsis-induced AKI. CLP-treated mice were used as an in vivo model of sepsis-induced AKI, and LPS-treated HK-2 and TCMK-1 cells were used as in vitro models. Bioinformatics analyses and mechanistic assays were utilized to reveal the relationships between molecules. H&amp;E staining was used to reveal morphological changes in kidney tissues. ELISAs were conducted to detect the concentrations of proinflammatory cytokines. We discovered that miR-155-5p was prominently upregulated in sepsis-induced AKI in vivo and in vitro. MiR-155-5p inhibition alleviated kidney injury in mice. Moreover, </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2026-04-25T03:27:24.502Z</modification><creation>2026-04-25T03:22:29.076Z</creation></dates><accession>S-EPMC11896158</accession><cross_references><pubmed>34431595</pubmed><doi>10.1002/kjm2.12442</doi></cross_references></HashMap>