ReviewFrontiers in immunology2013
Functions of NOD-Like Receptors in Human Diseases.
Review in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 4 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
166 citing papers in PubMed, 4 syntheses or guidelines pooled it, 317 citations in OpenAlex.
- Fever on hospital admission is associated with increased disease severity and mortality in acute pancreatitis: a systematic review and meta-analysis.Systematic reviews · 2026Pooled it
- The Role of NLRP3 Inflammasome in Obesity and PCOS-A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Co-occurrence of Asthma and the Inflammatory Bowel Diseases: A Systematic Review and Meta-analysis.Clinical and translational gastroenterology · 2018Pooled it
- Pooled it
- Chimeric vaccine based on Iraqi HLA alleles against a predominant localFrontiers in immunology · 2026Article
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Sensory Characteristics of Probiotic-Containing Foods: A Multidisciplinary Perspective on Enhancing Acceptability and Consumer Adherence.Nutrients · 2025Review
- Comprehensive Review of Mechanisms and Translational Perspectives on Programmed Cell Death in Vascular Calcification.Biomolecules · 2025Review
- Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.Journal of gastroenterology · 2025Review
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- Krill Oil Mitigates Cisplatin-Induced Ovarian Toxicity via Attenuation of Oxidative Stress and Inflammatory Pathways.Current issues in molecular biology · 2025Article
- Trim21 deficiency alleviates osteoporosis by inhibiting osteoclast differentiation through regulating Txnip.Arthritis research & therapy · 2025Article
- Differentially expressed circular RNAs and their diagnostic value in children with allergic rhinitis.The Journal of international medical research · 2025Article
- The Protective Role of Baicalin in the Regulation of NLRP3 Inflammasome in Different Diseases.Cell biochemistry and biophysics · 2025Review
- Targeting innate immune sensors for therapeutic strategies in infectious diseases.Journal of microbiology (Seoul, Korea) · 2025Review
- MST1 modulates inflammatory responses by targeting the NF-κB/NLRP3 pathway in LPS-induced acute lung injury.Histochemistry and cell biology · 2025Article
- Alloferon Mitigates LPS-Induced Endometritis by Attenuating the NLRP3/CASP1/IL-1β/IL-18 Signaling Cascade.Inflammation · 2025Article
- ImmunoMet Oncogenesis: A New Concept to Understand the Molecular Drivers of Cancer.Journal of clinical medicine · 2025Review
- Integrative transcriptomic analysis reveals diagnostic biomarkers for comorbidity of coronary artery disease and obstructive sleep apnea.Frontiers in cardiovascular medicine · 2025Article
- Updates on the Role of Innate Immunity's Pattern Recognition Receptors in Vitiligo Pathogenesis and Therapeutic Potential.Clinical, cosmetic and investigational dermatology · 2025Review
106 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide-binding and oligomerization domain NOD-like receptors (NLRs) are highly conserved cytosolic pattern recognition receptors that perform critical functions in surveying the intracellular environment for the presence of infection, noxious substances, and metabolic perturbations. Sensing of these danger signals by NLRs leads to their oligomerization into large macromolecular scaffolds and the rapid deployment of effector signaling cascades to restore homeostasis. While some NLRs operate by recruiting and activating inflammatory caspases into inflammasomes, others trigger inflammation via alternative routes including the nuclear factor-κB, mitogen-activated protein kinase, and regulatory factor pathways. The critical role of NLRs in development and physiology is demonstrated by their clear implications in human diseases. Mutations in the genes encoding NLRP3 or NLRP12 lead to hereditary periodic fever syndromes, while mutations in CARD15 that encodes NOD2 are linked to Crohn's disease or Blau's syndrome. Genome-wide association studies (GWASs) have identified a number of risk alleles encompassing NLR genes in a host of diseases including allergic rhinitis, multiple sclerosis, inflammatory bowel disease, asthma, multi-bacillary leprosy, vitiligo, early-onset menopause, and bone density loss in elderly women. Animal models have allowed the characterization of underlying effector mechanisms in a number of cases. In this review, we highlight the functions of NLRs in health and disease and discuss how the characterization of their molecular mechanisms provides new insights into therapeutic strategies for the management of inflammatory pathologies.
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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.