<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Merle NS</submitter><funding>Agence Nationale de la Recherche</funding><funding>CSL Behring</funding><funding>Institut National de la Santé et de la Recherche Médicale</funding><funding>Centre National de la Recherche Scientifique</funding><pagination>179</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5839160</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9</volume><pubmed_abstract>Intravascular erythrocyte destruction, accompanied by the release of pro-oxidative and pro-inflammatory components hemoglobin and heme, is a common event in the pathogenesis of numerous diseases with heterogeneous etiology and clinical features. A frequent adverse effect related to massive hemolysis is the renal injury and inflammation. Nevertheless, it is still unclear whether heme--a danger-associated molecular pattern--and ligand for TLR4 or upstream hemolysis-derived products are responsible for these effects. Well-characterized animal models of hemolysis with kidney impairment are needed to investigate how hemolysis drives kidney injury and to test novel therapeutic strategies. Here, we characterized the pathological processes leading to acute kidney injury and inflammation during mas</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis.</pubmed_title><pmcid>PMC5839160</pmcid><funding_grant_id>ANR JCJC––INFLACOMP 2015-2018 ANR-15-CE15-0001, ANR JCJC––COBIG ANR-13-JSV1-0006, ANR-11-IDEX-05-02 Recherche-USPC “HEMIR”</funding_grant_id><pubmed_authors>Grunenwald A</pubmed_authors><pubmed_authors>Frimat M</pubmed_authors><pubmed_authors>Rabant M</pubmed_authors><pubmed_authors>Gonnet F</pubmed_authors><pubmed_authors>Daugan M</pubmed_authors><pubmed_authors>Brinkman N</pubmed_authors><pubmed_authors>Noe R</pubmed_authors><pubmed_authors>Daniel R</pubmed_authors><pubmed_authors>Merle NS</pubmed_authors><pubmed_authors>Chauvet S</pubmed_authors><pubmed_authors>Miescher S</pubmed_authors><pubmed_authors>Figueres ML</pubmed_authors><pubmed_authors>Gentinetta T</pubmed_authors><pubmed_authors>Legros V</pubmed_authors><pubmed_authors>Knockaert S</pubmed_authors><pubmed_authors>Robe-Rybkine T</pubmed_authors><pubmed_authors>Roumenina LT</pubmed_authors><pubmed_authors>Houillier P</pubmed_authors><pubmed_authors>May O</pubmed_authors><pubmed_authors>Blanc-Brude OP</pubmed_authors><pubmed_authors>Dimitrov JD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis.</name><description>Intravascular erythrocyte destruction, accompanied by the release of pro-oxidative and pro-inflammatory components hemoglobin and heme, is a common event in the pathogenesis of numerous diseases with heterogeneous etiology and clinical features. A frequent adverse effect related to massive hemolysis is the renal injury and inflammation. Nevertheless, it is still unclear whether heme--a danger-associated molecular pattern--and ligand for TLR4 or upstream hemolysis-derived products are responsible for these effects. Well-characterized animal models of hemolysis with kidney impairment are needed to investigate how hemolysis drives kidney injury and to test novel therapeutic strategies. Here, we characterized the pathological processes leading to acute kidney injury and inflammation during mas</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018</publication><modification>2025-04-21T22:39:01.227Z</modification><creation>2019-03-26T23:17:54Z</creation></dates><accession>S-EPMC5839160</accession><cross_references><pubmed>29545789</pubmed><doi>10.3389/fimmu.2018.00179</doi></cross_references></HashMap>