ArticleFrontiers in pharmacology2023
ALDH2 attenuates myocardial pyroptosis through breaking down Mitochondrion-NLRP3 inflammasome pathway in septic shock.
Article in Frontiers in pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026Review
- Mitochondrial protein-enriched artificial nanovesicles: mitochondrial recovery and antioxidation for diabetic wound treatment.Journal of nanobiotechnology · 2026Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- ALDH2 in autophagy and cell death: molecular mechanisms and implications for diseases.Military Medical Research · 2025Review
- Wogonin attenuates septic cardiomyopathy by suppressing ALOX15-mediated ferroptosis.Acta pharmacologica Sinica · 2025Article
- Bifidobacterium longum Metabolite Indole-3-Carboxaldehyde Blocks HDAC3 and Inhibits Macrophage NLRP3 Inflammasome Activation in Intestinal Ischemia/Reperfusion Injury.Inflammation · 2025Article
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- Honokiol ameliorates pyroptosis in intestinal ischemia‑reperfusion injury by regulating the SIRT3‑mediated NLRP3 inflammasome.International journal of molecular medicine · 2025Article
- Therapeutic Targeting of Decr1 Ameliorates Cardiomyopathy by Suppressing Mitochondrial Fatty Acid Oxidation in Diabetic Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study.Journal of inflammation research · 2025Review
- Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.Journal of inflammation research · 2025Review
- ALDH2 Ameliorates Acute Gouty Arthritis Through Inhibiting NLRP3 Inflammasome and Pyroptosis by Nrf2/ROS Pathway.Journal of inflammation research · 2025Article
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- Resveratrol improved mitochondrial biogenesis by activating SIRT1/PGC-1α signal pathway in SAP.Scientific reports · 2024Article
- Frataxin Loss Promotes Angiotensin II-Induced Endothelial-to-Mesenchymal Transition.Journal of the American Heart Association · 2024Article
- An overview of the mechanisms and potential roles of extracellular vesicles in septic shock.Frontiers in immunology · 2023Review
- Current insight on the mechanisms of programmed cell death in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
18 authors.
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Abstract
Cell survival or death is critical for cardiac function. Myocardial pyroptosis, as a newly recognized programmed cell death, remains poorly understood in sepsis. In this study, we evaluated the effect of aldehyde dehydrogenase (ALDH2) on myocardial pyroptosis and revealed the underlying mechanisms in sepsis. We established a septic shock mice model by intraperitoneal injection of Lipopolysaccharide (LPS, 15 mg/kg) 12 h before sacrifice. It was found that aldehyde dehydrogenase significantly inhibited NOD-like receptor protein 3 (NLRP3) inflammasome activation and Caspase-1/GSDMD-dependent pyroptosis, which remarkably improved survival rate and septic shock-induced cardiac dysfunction, relative to the control group. While aldehyde dehydrogenase knockout or knockdown significantly aggravated these phenomena. Intriguingly, we found that aldehyde dehydrogenase inhibited LPS-induced deacetylation of Hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex α subunit (HADHA) by suppressing the translocation of Histone deacetylase 3 (HDAC3) from nuclei to mitochondria. Acetylated HADHA is essential for mitochondrial fatty acid β-oxidation, and its interruption can result in accumulation of toxic lipids, induce mROS and cause mtDNA and ox-mtDNA release. Our results confirmed the role of Histone deacetylase 3 and HADHA in NOD-like receptor protein 3 inflammasome activation.
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