ArticleAmerican journal of respiratory cell and molecular biology2017
Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction.
Article in American journal of respiratory cell and molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- DRD1 downregulation contributes to mechanical stretch-induced lung endothelial barrier dysfunction.Theranostics · 2021Trial
- Deciphering the Pathogenic Cascade of Acrolein-Induced Lung Injury: From Molecular Insult to Organ Failure.Journal of applied toxicology : JAT · 2026Article
- Acute lung injury and post-cardiac arrest syndrome: a narrative review.Journal of intensive care · 2024Review
- Countermeasures against Pulmonary Threat Agents.The Journal of pharmacology and experimental therapeutics · 2024Review
- Reduction in mitochondrial ROS improves oxidative phosphorylation and provides resilience to coronary endothelium in non-reperfused myocardial infarction.Basic research in cardiology · 2023Article
- Review
- Critical role of mitochondrial aldehyde dehydrogenase 2 in acrolein sequestering in rat spinal cord injury.Neural regeneration research · 2022Article
- Comparative study of oral versus parenteral crocin in mitigating acrolein-induced lung injury in albino rats.Scientific reports · 2022Article
- Neuroprotective effects of Alda-1 mitigate spinal cord injury in mice: involvement of Alda-1-induced ALDH2 activation-mediated suppression of reactive aldehyde mechanisms.Neural regeneration research · 2022Article
- CIGARETTE SMOKING INCREASES THE RISK OF ACUTE RESPIRATORY DISTRESS SYNDROME.Transactions of the American Clinical and Climatological Association · 2022Article
- Article
- GSNOR and ALDH2 alleviate traumatic spinal cord injury.Brain research · 2021Article
- Pharmacological Activation Of Aldehyde Dehydrogenase 2 Protects Against Heatstroke-Induced Acute Lung Injury by Modulating Oxidative Stress and Endothelial Dysfunction.Frontiers in immunology · 2021Article
- Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.American journal of respiratory cell and molecular biology · 2020Article
- Ginsenoside Rb1 reduces H2O2‑induced HUVEC dysfunction by stimulating the sirtuin‑1/AMP‑activated protein kinase pathway.Molecular medicine reports · 2020Article
- Alda-1 Attenuates Hyperoxia-Induced Acute Lung Injury in Mice.Frontiers in pharmacology · 2020Article
- In vitro profiling of endothelial volatile organic compounds under resting and pro-inflammatory conditions.Metabolomics : Official journal of the Metabolomic Society · 2019Article
- Fatty Acid Oxidation Protects against Hyperoxia-induced Endothelial Cell Apoptosis and Lung Injury in Neonatal Mice.American journal of respiratory cell and molecular biology · 2019Article
- Alda-1 Prevents Pulmonary Epithelial Barrier Dysfunction following Severe Hemorrhagic Shock through Clearance of Reactive Aldehydes.BioMed research international · 2019Article
- Cigarette Smoke Reduces Fatty Acid Catabolism, Leading to Apoptosis in Lung Endothelial Cells: Implication for Pathogenesis of COPD.Frontiers in pharmacology · 2019Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Inhalation of acrolein, a highly reactive aldehyde, causes lung edema. The underlying mechanism is poorly understood and there is no effective treatment. In this study, we demonstrated that acrolein not only dose-dependently induced lung edema but also promoted LPS-induced acute lung injury. Importantly, acrolein-induced lung injury was prevented and rescued by Alda-1, an activator of mitochondrial aldehyde dehydrogenase 2. Acrolein also dose-dependently increased monolayer permeability, disrupted adherens junctions and focal adhesion complexes, and caused intercellular gap formation in primary cultured lung microvascular endothelial cells (LMVECs). These effects were attenuated by Alda-1 and the antioxidant N-acetylcysteine, but not by the NADPH inhibitor apocynin. Furthermore, acrolein inhibited AMP-activated protein kinase (AMPK) and increased mitochondrial reactive oxygen species levels in LMVECs-effects that were associated with impaired mitochondrial respiration. AMPK total protein levels were also reduced in lung tissue of mice and LMVECs exposed to acrolein. Activation of AMPK with 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside blunted an acrolein-induced increase in endothelial monolayer permeability, but not mitochondrial oxidative stress or inhibition of mitochondrial respiration. Our results suggest that acrolein-induced mitochondrial dysfunction may not contribute to endothelial barrier dysfunction. We speculate that detoxification of acrolein by Alda-1 and activation of AMPK may be novel approaches to prevent and treat acrolein-associated acute lung injury, which may occur after smoke inhalation.
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