{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T11:08:57Z","timestamp":1782212937876,"version":"3.54.5"},"reference-count":22,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T00:00:00Z","timestamp":1768348800000},"content-version":"vor","delay-in-days":13,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100007924","name":"Bengbu Medical College","doi-asserted-by":"publisher","award":["2024byfy004"],"award-info":[{"award-number":["2024byfy004"]}],"id":[{"id":"10.13039\/501100007924","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007924","name":"Bengbu Medical College","doi-asserted-by":"publisher","award":["2024byfy005"],"award-info":[{"award-number":["2024byfy005"]}],"id":[{"id":"10.13039\/501100007924","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>The purpose of this study is to investigate the role of aldehyde dehydrogenase\u20102 (ALDH2) in septic myocardial injury, focusing on noncanonical pyroptosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In vivo, C57BL\/6J mice were divided into five groups: Sham, cecal ligation and puncture (CLP), CLP\u2009+\u2009Alda\u20101 (ALDH2 agonist), Sham\u2009+\u2009dimethyl sulfoxide (DMSO, solvent control), and CLP\u2009+\u2009DMSO. Cardiac function and histological\/ultrastructural changes were assessed via echocardiography, hematoxylin\u2013eosin (HE) staining, and transmission electron microscopy (TEM). Tumor necrosis factor\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      (TNF\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      ) and noncanonical pyroptosis\u2010related proteins (caspase\u201011, gasdermin\u2010D [GSDMD], high mobility group box 1 [HMGB1], and receptor for advanced glycation end products [RAGE]) were measured by enzyme\u2010linked immunosorbent assay (ELISA) and western blotting. Coimmunoprecipitation (CO\u2010IP) explored molecular mechanisms. In vitro, H9C2 cells were divided into six groups: Control, lipopolysaccharide (LPS)\u2010treated, ALDH2\u2010green fluorescent protein (GFP), LPS\u2009+\u2009ALDH2\u2010GFP, GFP, and GFP\u2009+\u2009LPS. Cell viability, lactate dehydrogenase (LDH) release, creatine kinase isoenzymes (CK\u2010MB), and target protein levels were detected via spectrophotometry, western blotting, and immunofluorescence (IF).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In vivo, Alda\u20101 significantly attenuated CLP\u2010induced cardiac dysfunction and reduced myocardial histological damage and ultrastructural impairment. In vitro, ALDH2 overexpression lowered LPS\u2010induced H9C2 cell viability, CK\u2010MB, and LDH release. Upregulating ALDH2 significantly reduced caspase\u201011, HMGB1, and RAGE expression. CO\u2010IP showed ALDH2 interacted with HMGB1, RAGE, and GSDMD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>ALDH2 protects the myocardium from septic injury by inhibiting caspase\u201011\u2010mediated noncanonical pyroptosis, possibly via direct interactions with GSDMD, HMGB1, and RAGE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/cdr\/5289405","type":"journal-article","created":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T08:41:07Z","timestamp":1768380067000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Aldehyde Dehydrogenase\u20102 Alleviates Septic Myocardial Injury by Inhibiting Caspase\u201011\u2010Mediated Noncanonical 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