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This study aims to determine the mechanisms by which alcohol consumption increases megamitochondria formation in the pathogenesis of ALD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results:<\/jats:title>\n                    <jats:p>\n                      Human alcoholic hepatitis (AH) liver samples were used for electron microscopy, histology, and biochemical analysis. Liver\u2010specific dynamin\u2010related protein 1 (DRP1; gene name\n                      <jats:italic toggle=\"yes\">DNM1L, an essential gene regulating mitochondria fission<\/jats:italic>\n                      ) knockout (L\u2010DRP1 KO) mice and wild\u2010type mice were subjected to chronic plus binge alcohol feeding. Both human AH and alcohol\u2010fed mice had decreased hepatic DRP1 with increased accumulation of hepatic megamitochondria. Mechanistic studies revealed that alcohol feeding decreased DRP1 by impairing transcription factor EB\u2013mediated induction of\n                      <jats:italic toggle=\"yes\">DNM1L<\/jats:italic>\n                      . L\u2010DRP1 KO mice had increased megamitochondria and decreased mitophagy with increased liver injury and inflammation, which were further exacerbated by alcohol feeding. Seahorse flux and unbiased metabolomics analysis showed alcohol intake increased mitochondria oxygen consumption and hepatic nicotinamide adenine dinucleotide (NAD\n                      <jats:sup>+<\/jats:sup>\n                      ), acylcarnitine, and ketone levels, which were attenuated in L\u2010DRP1 KO mice, suggesting that loss of hepatic DRP1 leads to maladaptation to alcohol\u2010induced metabolic stress. RNA\u2010sequencing and real\u2010time quantitative PCR analysis revealed increased gene expression of the cGAS\u2013stimulator of interferon genes (STING)\u2013interferon pathway in L\u2010DRP1 KO mice regardless of alcohol feeding. Alcohol\u2010fed L\u2010DRP1 KO mice had increased cytosolic mtDNA and mitochondrial dysfunction leading to increased activation of cGAS\u2010STING\u2010interferon signaling pathways and liver injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Alcohol consumption decreases hepatic DRP1 resulting in increased megamitochondria and mitochondrial maladaptation that promotes AH by mitochondria\u2010mediated inflammation and cell injury.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.32604","type":"journal-article","created":{"date-parts":[[2022,6,14]],"date-time":"2022-06-14T01:45:39Z","timestamp":1655171139000},"page":"159-175","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":119,"title":["Loss of hepatic DRP1 exacerbates alcoholic hepatitis by inducing megamitochondria and mitochondrial maladaptation"],"prefix":"10.1097","volume":"77","author":[{"given":"Xiaowen","family":"Ma","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luma","family":"Melo","sequence":"additional","affiliation":[{"name":"Center for Liver Diseases, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana","family":"Clemente\u2010Sanchez","sequence":"additional","affiliation":[{"name":"Center for Liver Diseases, Division 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