ArticleEuropean journal of pharmacology2019
Contribution of cathepsin B-dependent Nlrp3 inflammasome activation to nicotine-induced endothelial barrier dysfunction.
Article in European journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- The role of inflammation in the immune evasion of KRas.Frontiers in immunology · 2026Review
- Contribution of NLRP3-GSDMD axis to PDGF-BB-induced vascular smooth muscle cell phenotypic transition.American journal of physiology. Cell physiology · 2025Article
- NLRP3-Mediated PANoptosis and Associated Interventions in Endothelial Injury.Cardiovascular toxicology · 2025Review
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Cathepsin B in urological tumors: unraveling its role and therapeutic potential.Discover oncology · 2025Review
- Exosomal novel-miRNA-126 mediates vascular endothelial dysfunction by targeting AhR-NLRP3 pathway in nonalcoholic steatohepatitis.Scientific reports · 2025Article
- Article
- Exosomes in arteriovenous fistula stenosis.Frontiers in cell and developmental biology · 2025Review
- Tetrahydrocurcumin Protects Microglial Cells AgainstInternational journal of medical sciences · 2025Article
- Bridging inflammation and venous thrombosis: the NLRP3 inflammasome connection.Frontiers in cardiovascular medicine · 2025Review
- Suppression of cathepsin B attenuates myocardial injury via limiting cardiomyocyte apoptosis.Open medicine (Warsaw, Poland) · 2025Article
- Coronary Microvascular Dysfunction Is Associated With Augmented Lysosomal Signaling in Hypercholesterolemic Mice.Journal of the American Heart Association · 2024Article
- Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.Journal of cellular and molecular medicine · 2024Review
- Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.bioRxiv : the preprint server for biology · 2024Article
- The impacts of tobacco and nicotine on HIV-1 infection, inflammation, and the blood-brain barrier in the central nervous system.Frontiers in pharmacology · 2024Review
- Cathepsin B S-nitrosylation promotes ADAR1-mediated editing of its own mRNA transcript via an ADD1/MATR3 regulatory axis.Cell research · 2023Article
- Trimethylamine N-Oxide (TMAO) Inducing Endothelial Injury: UPLC-MS/MS-Based Quantification and the Activation of Cathepsin B-Mediated NLRP3 Inflammasome.Molecules (Basel, Switzerland) · 2023Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- What type of cell death occurs in chronic cerebral hypoperfusion? A review focusing on pyroptosis and its potential therapeutic implications.Frontiers in cellular neuroscience · 2023Review
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Recent studies indicate that endothelial Nlrp3 inflammasome is critically involved in the development of cardiovascular complications. However, it remains unknown whether endothelial inflammasome is involved in endothelial barrier dysfunction associated with smoking. This study aims to investigate the role of endothelial Nlrp3 inflammasome in nicotine-induced disruption of inter-endothelial tight junctions and consequent endothelial barrier dysfunction. The confocal microscopic analysis demonstrated that mice treated with nicotine exhibited disrupted inter-endothelial tight junctions as shown by decreased ZO-1 and ZO-2 expression in the coronary arterial endothelium, whereas the decreases in ZO-1/2 were prevented by Nlrp3 gene deficiency. In cultured endothelial cells, nicotine caused Nlrp3 inflammasome complex formation and enhances the inflammasome activity as shown by increased cleavage of pro-caspase-1, and interleukin-1β (IL-1β) production. Further, nicotine disrupted tight junction and increased permeability in an endothelial cell monolayer, and this nicotine-induced effect was prevented by silencing of Nlrp3 gene, inhibition of caspase-1, or blockade of high mobility group box 1 (HMGB1). Nicotine increased endothelial cell lysosomal membrane permeability and triggered the lysosomal release of cathepsin B, whereas these events were prevented by pretreating cells with a lysosome stabilizing agent, dexamethasone. Collectively, our data suggest that nicotine enhances cathepsin B-dependent Nlrp3 inflammasome activation and the consequent production of a novel permeability factor HMGB1, which causes disruption of inter-endothelial tight junctions leading to endothelial hyperpermeability. Instigation of endothelial inflammasomes may serve as an important pathogenic mechanism contributing to the early onset of vasculopathy associated with smoking.
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