ArticleCardiovascular therapeutics2026
Aldehyde Dehydrogenase-2 Alleviates Septic Myocardial Injury by Inhibiting Caspase-11-Mediated Noncanonical Pyroptosis.
Article in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Aldehyde Dehydrogenase-2 Alleviates Septic Myocardial Injury by Inhibiting Caspase-11-Mediated Noncanonical Pyroptosis.Cardiovascular therapeutics · 2026Article
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Purpose: The purpose of this study is to investigate the role of aldehyde dehydrogenase-2 (ALDH2) in septic myocardial injury, focusing on noncanonical pyroptosis. Methods: In vivo, C57BL/6J mice were divided into five groups: Sham, cecal ligation and puncture (CLP), CLP + Alda-1 (ALDH2 agonist), Sham + dimethyl sulfoxide (DMSO, solvent control), and CLP + DMSO. Cardiac function and histological/ultrastructural changes were assessed via echocardiography, hematoxylin-eosin (HE) staining, and transmission electron microscopy (TEM). Tumor necrosis factor- Results: In vivo, Alda-1 significantly attenuated CLP-induced cardiac dysfunction and reduced myocardial histological damage and ultrastructural impairment. In vitro, ALDH2 overexpression lowered LPS-induced H9C2 cell viability, CK-MB, and LDH release. Upregulating ALDH2 significantly reduced caspase-11, HMGB1, and RAGE expression. CO-IP showed ALDH2 interacted with HMGB1, RAGE, and GSDMD. Conclusion: ALDH2 protects the myocardium from septic injury by inhibiting caspase-11-mediated noncanonical pyroptosis, possibly via direct interactions with GSDMD, HMGB1, and RAGE.
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