{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T18:37:14Z","timestamp":1790707034519,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,8,15]],"date-time":"2025-08-15T00:00:00Z","timestamp":1755216000000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","award":["ANR\u201023\u2010CE14\u20100063\u201001"],"award-info":[{"award-number":["ANR\u201023\u2010CE14\u20100063\u201001"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sepsis survivors often experience sustained muscle weakness, leading to physical disability, with no pharmacological treatments available. Despite these well\u2010documented long\u2010term clinical consequences, research exploring the cellular and molecular mechanisms is sorely lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Bioinformatic analysis was performed in the\n                      <jats:italic>vastus lateralis<\/jats:italic>\n                      transcriptome of human ICU survivors 7\u2009days after ICU discharge (D7), 6\u2009months (M6) and age\u2010 and sex\u2010matched controls. Enrichment analysis using Gene Ontology (GO) terms and Mitocarta3.0 was performed at D7 and M6 on differentially expressed genes (DEGs) and modules identified by weighted gene co\u2010expression network analysis (WGCNA). Using a murine model of resuscitated sepsis induced by caecal slurry injection, pathways identified by the bioinformatics analysis were explored in 18\u2010 to 24\u2010week\u2010old sepsis\u2010surviving (SS) mice at Day 10. Autophagy flux was investigated both in\u00a0vivo and in\u00a0vitro with chloroquine, a lysosomal inhibitor and urolithin A (UA), an autophagy inducer. Systemic metabolism was evaluated with indirect calorimetry, muscle phenotype with in\u00a0situ and ex\u00a0vivo contractility, muscle mass, myofibre cross\u2010sectional area and typing and mitochondrial population with transmission electron microscopy (TEM), as well as mitochondrial function with high\u2010resolution respirometry. Autophagic vacuole (AV) level was monitored using LC3B\u2010II and P62 protein expression and TEM.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pathways related to \u2018mitochondrion\u2019 were the only ones whose deregulation persisted between D7 and M6 (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05) and characterized WGCNA modules correlated with muscle mass, strength and physical function. Shared mitochondrial DEGs between D7 and M6 encoded matrix mitochondrial proteins related to \u2018metabolism\u2019 and \u2018mitochondrial dynamics\u2019. SS mice exhibited reduced complex I\u2010driven oxygen consumption (CI\u2010J\n                      <jats:sub>O2<\/jats:sub>\n                      ) (\u221245%), increased S\u2010nitrosylation of complex I, damaged (+35%) and oxidized (+51%) mitochondria and AV accumulation (5 vs. 50 AVs\/mm\n                      <jats:sup>2<\/jats:sup>\n                      ) compared with sham pair\u2010fed mice (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05) despite no differences in mitochondrial size or number. Autophagy flux was reduced in SS mice due to decreased AV degradation ratio (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). UA restored a balanced autophagy flux (turnover ratio 0.96 vs. \u22120.17) by increasing AVs formation and degradation ratio (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). UA also improved CI\u2010J\n                      <jats:sub>O2<\/jats:sub>\n                      (81 vs. 106\u2009pmol\/s\/mg), tetanic force (215 vs. 244 mN\/mm\n                      <jats:sup>2<\/jats:sup>\n                      ) and hindlimb muscle weight in SS mice (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Mitochondrial and autophagy disruption contributes to long\u2010term muscle dysfunction in human and mouse sepsis survivors. We demonstrate for the first time that sepsis induces an autophagy flux blockade. Urolithin A prevents mitochondrial and muscle impairments both in\u00a0vivo and in\u00a0vitro by improving autophagy flux.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcsm.70041","type":"journal-article","created":{"date-parts":[[2025,8,16]],"date-time":"2025-08-16T04:27:21Z","timestamp":1755318441000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Sepsis Induces Long\u2010Term Muscle and Mitochondrial Dysfunction due to Autophagy Disruption Amenable by Urolithin A"],"prefix":"10.1002","volume":"16","author":[{"given":"Alexandre","family":"Pierre","sequence":"first","affiliation":[{"name":"Univ. 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