ReviewAntioxidants (Basel, Switzerland)2022
NLRP3 Inflammasome in Vascular Disease: A Recurrent Villain to Combat Pharmacologically.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Vascular smooth muscle-specific NLRP3 hyperactivation exacerbates arterial intimal hyperplasia in mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Immunotherapy for depression: targeting cytokine pathways in major depressive disorder.Psychopharmacology · 2026Review
- Vascular Smooth Muscle-Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in Mice.Research square · 2026Article
- Aging-driven metabolic abnormalities remodel intercellular communication through the gut-liver-heart axis and may promote coronary artery disease: the key role of bile acid metabolism.Frontiers in immunology · 2026Review
- Sirtuin 2 regulates NOD-like receptor protein 3/nuclear factor kappa B axis to promote cartilage repair in osteoarthritis.Journal of cell communication and signaling · 2025Article
- Unveiling the molecular and cellular links between obstructive sleep apnea-hypopnea syndrome and vascular aging.Chinese medical journal · 2025Review
- Oral Angiotensin-(1-7) formulation after established elastase-induced emphysema suppresses inflammation and restores lung architecture.Frontiers in pharmacology · 2025Article
- Mechanisms Underlying Vascular Inflammaging: Current Insights and Potential Treatment Approaches.Aging and disease · 2024Review
- Aerobic Exercise Attenuates Doxorubicin-Induced Cardiomyopathy by Suppressing NLRP3 Inflammasome Activation in a Rat Model.International journal of molecular sciences · 2024Article
- Review
- Forsythoside B alleviates cerebral ischemia-reperfusion injury via inhibiting NLRP3 inflammasome mediated by SIRT1 activation.PloS one · 2024Article
- Selective NLRP3 Inflammasome Inhibitor MCC950 Suppresses Inflammation and Facilitates Healing in Vascular Materials.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Portrayal of NLRP3 Inflammasome in Atherosclerosis: Current Knowledge and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Special Issue "Oxidative Stress in Aging and Associated Chronic Diseases".Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the great advances in medicine, mortality from cardiovascular diseases keeps on growing. This tendency is not likely to change considering the pandemic proportions of obesity and diabetes. Besides, the global population is more aged as life expectancy increases, and vascular aging plays a key role in the increased risk of vascular disease. In light of recent trials, namely the CANTOS study, showing the enormous potential of anti-inflammatory therapies and in particular those targeted to IL-1β, a change in therapeutical management of cardiovascular diseases is coming about. The NLRP3 inflammasome is a multiprotein complex that assembles to engage the innate immune defense by processing the maturation of pro-inflammatory cytokines IL-1β and IL-18. Substantial evidence has positioned the NLRP3 inflammasome at the center of vascular disease progression, with a particular significance in the context of aging and the low-grade chronic inflammation associated (inflammaging). Therefore, pharmacological blockade of the NLRP3 inflammasome and its end products has arisen as an extremely promising tool to battle vascular disease. In this review, we discuss the mechanisms by which the NLRP3 inflammasome contributes to vascular disease, with particular attention to the consequences of aging, and we enumerate the therapeutic options available to combat this recurrent villain.
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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.