<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>2022</volume><submitter>Yang B</submitter><pubmed_abstract>Current evidences indicate that both inflammation and oxidative stress contribute to the pathogenesis of sepsis-associated skeletal muscle atrophy. However, the interaction between inflammation and oxidative stress has not been completely understood in sepsis-associated skeletal muscle atrophy. Here in the present study, a murine model of sepsis has been established by cecal ligation and puncture (CLP) with wild-type and interleukin- (IL-) 6 knockout (KO) mice. Our results suggested that IL-6 KO largely attenuated skeletal muscle atrophy as reflected by reduced protein degradation, increased cross-sectional area (CSA) of myofibers, and improved muscle contractile function (all &lt;i>P&lt;/i> &lt; 0.05). In addition, we observed that IL-6 KO promoted the expression of peroxisome proliferator-activat</pubmed_abstract><journal>Oxidative medicine and cellular longevity</journal><pagination>9148246</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9068301</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-6 Deficiency Attenuates Skeletal Muscle Atrophy by Inhibiting Mitochondrial ROS Production through the Upregulation of PGC-1&lt;i>α&lt;/i> in Septic Mice.</pubmed_title><pmcid>PMC9068301</pmcid><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Yang B</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Shi J</pubmed_authors><pubmed_authors>Shen Y</pubmed_authors><pubmed_authors>Chen R</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-6 Deficiency Attenuates Skeletal Muscle Atrophy by Inhibiting Mitochondrial ROS Production through the Upregulation of PGC-1&lt;i>α&lt;/i> in Septic Mice.</name><description>Current evidences indicate that both inflammation and oxidative stress contribute to the pathogenesis of sepsis-associated skeletal muscle atrophy. However, the interaction between inflammation and oxidative stress has not been completely understood in sepsis-associated skeletal muscle atrophy. Here in the present study, a murine model of sepsis has been established by cecal ligation and puncture (CLP) with wild-type and interleukin- (IL-) 6 knockout (KO) mice. Our results suggested that IL-6 KO largely attenuated skeletal muscle atrophy as reflected by reduced protein degradation, increased cross-sectional area (CSA) of myofibers, and improved muscle contractile function (all &lt;i>P&lt;/i> &lt; 0.05). In addition, we observed that IL-6 KO promoted the expression of peroxisome proliferator-activat</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-26T15:14:49.065Z</modification><creation>2024-11-20T20:31:27.526Z</creation></dates><accession>S-EPMC9068301</accession><cross_references><pubmed>35528525</pubmed><doi>10.1155/2022/9148246</doi></cross_references></HashMap>