ArticleProceedings of the National Academy of Sciences of the United States of America2017
Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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161 citing papers in PubMed, 259 citations in OpenAlex.
- Whole-genome sequencing identifies genetic diversity and adaptive signatures of hypoxia and ultraviolet radiation in Chinese chickens.Journal of advanced research · 2026Article
- Capsanthin Attenuates Osteoporosis by Targeting the Urotensin II Receptor Pathway to Inhibit Oxidative Stress and NLRP3 Inflammasome Activation.Calcified tissue international · 2026Article
- Pathological, diagnostic, and therapeutic implications of non-coding RNAs in deep vein thrombosis: A comprehensive review.Journal of thrombosis and thrombolysis · 2026Review
- Long non-coding RNA LINC00607 epigenetically regulates endothelial TSPAN18 to promote hypoxia-induced thromboinflammation.The Journal of biological chemistry · 2026Article
- Platelet-driven monocyte activation promotes hypoxic thromboinflammation through the HIF-1α-NLRP3-EGR-1 axis.Haematologica · 2026Article
- Hypoxia-inducible factors contribute to venous thrombosis in a mouse model of myeloproliferative neoplasms.Blood advances · 2026Article
- The Role of Immune Infiltration and Oxidative Stress in the Progression of Cerebral Cavernous Malformation.Brain and behavior · 2026Review
- Artificial Intelligence-Driven Integration of ECG and Molecular Biomarkers in Pulmonary Embolism.International journal of molecular sciences · 2026Review
- Insights Into the HIF-1α-Mediated NLRP3 Pyroptosis Pathway in the Regulation of Musculoskeletal Diseases in the High-Altitude Environment.Journal of inflammation research · 2026Review
- Free and Total Thyroxine Levels are Associated with Cardiovascular-Kidney-Metabolic Syndrome Stages in Elderly Cohorts from China and the United States: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- High-altitude thrombosis: divergent pathophysiological mechanisms and preventive strategies in acutely exposed population and native highlanders.Frontiers in cardiovascular medicine · 2026Review
- Analysis of risk factors for calf muscular vein thrombosis in elderly patients with acute exacerbation of chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2026Article
- Immune drivers of venous thrombosis: orchestrating initiation, formation, and resolution within the hypoxic microenvironment.Frontiers in immunology · 2026Review
- Antithrombin in Hyperuricemic Nephropathy: Unveiling Its Noncanonical Renoprotective Roles and Therapeutic Repurposing Potential.Kidney & blood pressure research · 2026Review
- Toward targeting of inflammasome signaling in venous thrombosis.Journal of thrombosis and haemostasis : JTH · 2025Review
- Factor XI and Cancer: Physiopathological Linkage and Clinical Perspectives.Journal of clinical medicine · 2025Review
- Intermittent hypoxia aggravates asthma inflammation via NLRP3/IL-1β-dependent pyroptosis mediated by HIF-1α signalling pathway.Chinese medical journal · 2025Article
- Oxidative Stress and Inflammation in Hypoxemic Respiratory Diseases and Their Comorbidities: Molecular Insights and Diagnostic Advances in Chronic Obstructive Pulmonary Disease and Sleep Apnea.Antioxidants (Basel, Switzerland) · 2025Review
- Hypoxia drives progression of multiple sclerosis by enhancing the inflammasome activation in macrophages with Porphyromonas gingivalis infection.Cell death discovery · 2025Article
- Disseminated intravascular coagulation.Journal of intensive care · 2025Review
101 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Venous thromboembolism (VTE), caused by altered hemostasis, remains the third most common cause of mortality among all cardiovascular conditions. In addition to established genetic and acquired risk factors, low-oxygen environments also predispose otherwise healthy individuals to VTE. Although disease etiology appears to entail perturbation of hemostasis pathways, the key molecular determinants during immediate early response remain elusive. Using an established model of venous thrombosis, we here show that systemic hypoxia accelerates thromboembolic events, functionally stimulated by the activation of nucleotide binding domain, leucine-rich-containing family, pyrin domain containing 3 (NLRP3) inflammasome complex and increased IL-1β secretion. Interestingly, we also show that the expression of NLRP3 is mediated by hypoxia-inducible factor 1-alpha (HIF-1α) during these conditions. The pharmacological inhibition of caspase-1, in vivo knockdown of NLRP3, or HIF-1α other than IL-1β-neutralizing antibodies attenuated inflammasome activation and curtailed thrombosis under hypoxic conditions. We extend the significance of these preclinical findings by studying modulation of this pathway in patients with altitude-induced venous thrombosis. Our results demonstrate distinctive, increased expression of NLRP3, caspase-1, and IL-1β in individuals with clinically established venous thrombosis. We therefore propose that an early proinflammatory state in the venous milieu, orchestrated by the HIF-induced NLRP3 inflammasome complex, is a key determinant of acute thrombotic events during hypoxic conditions.
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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.