ArticleOncotarget2016
Enhancement of endothelial permeability by free fatty acid through lysosomal cathepsin B-mediated Nlrp3 inflammasome activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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The trial behind it
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Who cites it
76 citing papers in PubMed, 113 citations in OpenAlex.
- Exploring the Potential of Calebin-A in Targeting Obesity-Related Genes and Pathways.Journal of cellular and molecular medicine · 2026Article
- Dietary Saturated Fatty Acids as Evolutionarily Conserved Signals of Immune Activation.DNA and cell biology · 2026Review
- Conformable Device for Independent Measurements of Mucosal and Vascular Barriers in a Complex In Vitro Intestinal Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The NLRP3 inflammasome in metabolic dysfunction-associated steatotic liver disease: role and advances in therapeutic targeting.Frontiers in immunology · 2026Review
- Discovery of Personalized Treatment for Immuno-Metabolic Depression-Focus on 11beta Hydroxysteroid Dehydrogenase Type 2 (11betaHSD2) and Toll-like Receptor 4 (TLR4) Inhibition with Enoxolone.Pharmaceuticals (Basel, Switzerland) · 2025Review
- RfeA from Streptococcus suis serotype 2 triggers NLRP3/Caspase-1-dependent pyroptosis leading to blood-brain barrier disruption.Veterinary research · 2025Article
- Contribution of NLRP3-GSDMD axis to PDGF-BB-induced vascular smooth muscle cell phenotypic transition.American journal of physiology. Cell physiology · 2025Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Review
- Case Report: Non-Catheter-Related arterial hemorrhage as a complication of hemoperfusion in hypertriglyceridemic pancreatitis: mechanistic hypotheses and multidisciplinary strategies.Frontiers in medicine · 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
- ER stress inhibition enhances formation of triacylglcerols and protects endothelial cells from lipotoxicity.Cell communication and signaling : CCS · 2024Article
- Shear Stress and the AMP-Activated Protein Kinase Independently Protect the Vascular Endothelium from Palmitate Lipotoxicity.Biomedicines · 2024Article
- Cellular metabolism changes in atherosclerosis and the impact of comorbidities.Frontiers in cell and developmental biology · 2024Review
- Overview of multifunctional cysteinyl cathepsins in atherosclerosis-based cardiovascular disease: from insights into molecular functions to clinical implications.Cell & bioscience · 2023Review
- 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 Role of Palmitic Acid in the Co-Toxicity of Bacterial Metabolites to Endothelial Cells.Vascular health and risk management · 2023Article
- All Roads Lead to Cathepsins: The Role of Cathepsins in Non-Alcoholic Steatohepatitis-Induced Hepatocellular Carcinoma.Biomedicines · 2022Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Obesity is an important risk factor for exacerbating chronic diseases such as cardiovascular disease and cancer. High serum level of saturated free fatty acids such as palmitate is an important contributor for obesity-induced diseases. Here, we examined the contribution of inflammasome activation in vascular cells to free fatty acid-induced endothelial dysfunction and vascular injury in obesity. Our findings demonstrated that high fat diet-induced impairment of vascular integrity and enhanced vascular permeability in the myocardium in mice were significantly attenuated by Nlrp3 gene deletion. In microvascular endothelial cells (MVECs), palmitate markedly induces Nlrp3 inflammasome complex formation leading to caspase-1 activation and IL1β production. By fluorescence microscopy and flow cytometry, we observed that such palmitate-induced Nlrp3 inflammasome activated was accompanied by a reduction in inter-endothelial tight junction proteins ZO-1/ZO-2. Such palmitate-induced decrease of ZO-1/ZO-2 was also correlated with an increase in the permeability of endothelial monolayers treated with palmitates. Moreover, palmitate-induced alterations in ZO-1/ZO-2 or permeability were significantly reversed by an inflammasome activity inhibitor, YVAD, or a high mobility group box 1 (HMGB1) activity inhibitor glycyrrhizin. Lastly, blockade of cathepsin B with Ca-074Me significantly abolished palmitate-induced activation of Nlrp3 inflammasomes, down-regulation of ZO-1/ZO-2, and enhanced permeability in MVECs or their monolayers. Together, these data strongly suggest that activation of endothelial inflammasomes due to increased free fatty acids produces HMGB1, which disrupts inter-endothelial junctions and increases paracellular permeability of endothelium contributing to early onset of endothelial injury during obesity.
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Registered trials
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.