ReviewFrontiers in immunology2022
Activation and Regulation of NLRP3 by Sterile and Infectious Insults.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Cell-specific exosomes in sepsis-associated ARDS: from immunometabolic reprogramming to precision medicine.Frontiers in immunology · 2026Review
- Research advances on NLRP3 inflammasomes in organ transplantation.Frontiers in immunology · 2026Review
- Genetic removal of Nlrp3 protects against age-related and R345W Efemp1-induced basal laminar deposit formation.Cell death & disease · 2025Article
- Protective Effect of Neochlorogenic Acid on Diabetic Nephropathy via Inflammation and Pyroptosis Suppression.Journal of agricultural and food chemistry · 2025Article
- Exploring extracellular vesicles as novel therapeutic agents for intervertebral disc degeneration: delivery, applications, and mechanisms.Stem cell research & therapy · 2025Review
- Effect and mechanism of T lymphocytes on human induced pluripotent stem cell-derived cardiomyocytes via Proteomics.Stem cell research & therapy · 2024Article
- Deciphering the link: ferroptosis and its role in glioma.Frontiers in immunology · 2024Review
- Chalcone: A potential scaffold for NLRP3 inflammasome inhibitors.European journal of medicinal chemistry reports · 2023Article
- Neutrophil Extracellular Traps Release following Hypoxic-Ischemic Brain Injury in Newborn Rats Treated with Therapeutic Hypothermia.International journal of molecular sciences · 2023Article
- The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury.International journal of molecular sciences · 2023Review
- What are NLRP3-ASC specks? an experimental progress of 22 years of inflammasome research.Frontiers in immunology · 2023Review
- Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2022Review
- NLRP3+ macrophages aggravate inflammatory cystitis in diabetes.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nod-Like Receptor (NLR) is the largest family of Pathogen Recognition Receptors (PRRs) that patrols the cytosolic environment. NLR engagement drives caspase-1 activation that cleaves pro-IL-1B which then gets secreted. Released IL-1B recruits immune cells to the site of infection/injury. Caspase-1 also cleaves Gasdermin-D (GSDM-D) that forms pores within the plasma membrane driving inflammatory cell death called pyroptosis. NLRP3 is the most extensively studied NLR. The NLRP3 gene is encoded by 9 exons, where exon 1 codes for pyrin domain, exon 3 codes for NACHT domain, and Leucine Rich Repeat (LRR) domain is coded by exon 4-9. Exon 2 codes for a highly disorganized loop that connects the rest of the protein to the pyrin domain and may be involved in NLRP3 regulation. The NLRP3 inflammasome is activated by many structurally divergent agonists of microbial, environmental, and host origin. Activated NLRP3 interacts with an adaptor protein, ASC, that bridges it to pro-Caspase-1 forming a multi-protein complex called inflammasome. Dysregulation of NLRP3 inflammasome activity is a hallmark of pathogenesis in several human diseases, indicating its highly significant clinical relevance. In this review, we summarize the existing knowledge about the mechanism of activation of NLRP3 and its regulation during activation by infectious and sterile triggers.
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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.