ArticleBiochimica et biophysica acta2015
Endothelial Nlrp3 inflammasome activation associated with lysosomal destabilization during coronary arteritis.
Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 104 citations in OpenAlex.
- Membrane Raft Redox Signaling Mediates Trimethylamine N-Oxide-Induced NLRP3 Inflammasome Activation and Endothelial Dysfunction.Antioxidants (Basel, Switzerland) · 2026Article
- Preclinical evaluation of cysteine protease-inhibitor aloxistatin (E64d) for heart failure therapy.Journal of molecular medicine (Berlin, Germany) · 2026Article
- A new paradigm: 46 structural cell types function as environment-supporting innate immune cells, with endothelial and vascular smooth muscle cells as key prototypes.iNew medicine · 2026Article
- Article
- The Link Between Endoplasmic Reticulum Stress and Lysosomal Dysfunction Under Oxidative Stress in Cancer Cells.Biomolecules · 2025Review
- Revealing the dance of NLRP3: spatiotemporal patterns in inflammasome activation.Immunometabolism (Cobham, Surrey) · 2025Review
- Coronary Microvascular Dysfunction Is Associated With Augmented Lysosomal Signaling in Hypercholesterolemic Mice.Journal of the American Heart Association · 2024Article
- Disulfiram attenuates cell and tissue damage and blood‒brain barrier dysfunction after intracranial haemorrhage by inhibiting the classical pyroptosis pathway.Scientific reports · 2024Article
- Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.International journal of molecular sciences · 2024Review
- The Future of Kawasaki Disease Diagnosis: Liquid Biopsy May Hold the Key.International journal of molecular sciences · 2024Review
- Coronary Microvascular Dysfunction is Associated with Augmented Lysosomal Signaling in Hypercholesterolemic Mice.bioRxiv : the preprint server for biology · 2024Article
- Article
- Real-Time Monitoring of Lysosomal Membrane Permeabilization Using Acridine Orange.Methods and protocols · 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
- Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.Biochemistry and biophysics reports · 2023Review
- Resistance of hypervirulentFrontiers in immunology · 2023Article
- The Impact of Cytokines in Coronary Atherosclerotic Plaque: Current Therapeutic Approaches.International journal of molecular sciences · 2022Review
- Shared Inflammatory Pathology of Stroke and COVID-19.International journal of molecular sciences · 2022Review
- The Evolving Role of Nucleotide-binding Oligomerisation Domain-like Receptor Pyrin Domain 3 Inflammasome Activation in Vascular Endothelial Cells: A Review.The Malaysian journal of medical sciences : MJMS · 2022Review
- Elevated CTSL Gene Expression Correlated with Proinflammatory Cytokines in Omental Adipose Tissue of Patients with Obesity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Inflammasomes play a critical role in the development of vascular diseases. However, the molecular mechanisms activating the inflammasome in endothelial cells and the relevance of this inflammasome activation is far from clear. Here, we investigated the mechanisms by which an Nlrp3 inflammasome is activated to result in endothelial dysfunction during coronary arteritis by Lactobacillus casei (L. casei) cell wall fragments (LCWE) in a mouse model for Kawasaki disease. Endothelial dysfunction associated with increased vascular cell adhesion protein 1 (VCAM-1) expression and endothelial-leukocyte adhesion was observed during coronary arteritis in mice treated with LCWE. Accompanied with these changes, the inflammasome activation was also shown in coronary arterial endothelium, which was characterized by a marked increase in caspase-1 activity and IL-1β production. In cultured endothelial cells, LCWE induced Nlrp3 inflammasome formation, caspase-1 activation and IL-1β production, which were blocked by Nlrp3 gene silencing or lysosome membrane stabilizing agents such as colchicine, dexamethasone, and ceramide. However, a potassium channel blocker glibenclamide or an oxygen free radical scavenger N-acetyl-l-cysteine had no effects on LCWE-induced inflammasome activation. LCWE also increased endothelial cell lysosomal membrane permeability and triggered lysosomal cathepsin B release into cytosol. Silencing cathepsin B blocked LCWE-induced Nlrp3 inflammasome formation and activation in endothelial cells. In vivo, treatment of mice with cathepsin B inhibitor also abolished LCWE-induced inflammasome activation in coronary arterial endothelium. It is concluded that LCWE enhanced lysosomal membrane permeabilization and consequent release of lysosomal cathepsin B, resulting in activation of the endothelial Nlrp3 inflammasome, which may contribute to the development of coronary arteritis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.