ReviewFrontiers in immunology2014
Genetic Susceptibility to ANCA-Associated Vasculitis: State of the Art.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 35 citations in OpenAlex.
- Familial associations between ANCA-associated vasculitis and other immune-mediated inflammatory diseases: a case control study.Rheumatology international · 2026Article
- Microscopic Polyangiitis Following Kawasaki Disease in a Patient With Autoimmune Predisposition.Cureus · 2026Article
- Pediatric ANCA-Associated Vasculitis: Variable Clinical Course in a Case Series of Three Patients and Literature Review.Children (Basel, Switzerland) · 2026Article
- Potential impact of two functional variants in theCaspian journal of internal medicine · 2026Article
- Immunopathology of Antineutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis.International journal of molecular sciences · 2025Review
- Dual pathogenesis and treatment approaches for eosinophilic granulomatosis with polyangiitis: a comprehensive review.Reumatologia · 2025Review
- Refractory Eosinophilic Granulomatosis with Polyangiitis Complicated with IgG4-related Disease Showing Different Treatment Responses for Each Organ.Internal medicine (Tokyo, Japan) · 2023Article
- Familial Association of Granulomatosis With Polyangiitis: A Case-Based Review of Literature.Cureus · 2023Article
- Diagnostic and Therapeutic Approach in ANCA-Associated Glomerulonephritis: A Review on Management Strategies.Frontiers in medicine · 2022Review
- T cell plasticity in renal autoimmune disease.Cell and tissue research · 2021Review
- Unraveling the Immunopathogenesis and Genetic Variants in Vasculitis Toward Development of Personalized Medicine.Frontiers in cardiovascular medicine · 2021Review
- Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Update: Genetic Pathogenesis.Frontiers in immunology · 2021Review
- Contributions of Eosinophils to Human Health and Disease.Annual review of pathology · 2020Review
- Novel insights into the aetiology of granulomatosis with polyangiitis-a case-control study using the Clinical Practice Research Datalink.Rheumatology (Oxford, England) · 2018Article
- Eosinophils from Physiology to Disease: A Comprehensive Review.BioMed research international · 2018Review
- Eosinophils in Autoimmune Diseases.Frontiers in immunology · 2017Review
- Heterogeneity and individualized therapy for eosinophilic granulomatosis with polyangiitis.Therapeutic advances in respiratory diseaseReview
- Therapeutic Complement Targeting in ANCA-Associated Vasculitides and Thrombotic Microangiopathy.Biomedicine hubReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ANCA-associated vasculitis (AAV) is a group of disorders that is caused by inflammation affecting small blood vessels. Both arteries and veins are affected. AAV includes microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA) renamed from Wegener's granulomatosis, and eosinophilic granulomatosis with polyangiitis (EGPA), renamed from Churg-Strauss syndrome. AAV is primarily due to leukocyte migration and resultant damage. Despite decades of research, the mechanisms behind AAV disease etiology are still not fully understood, although it is clear that genetic and environmental factors are involved. To improve the understanding of the disease, the genetic component has been extensively studied by candidate association studies and two genome-wide association studies. The majority of the identified genetic AAV risk factors are common variants. These have uncovered information that still needs further investigation to clarify its importance. In this review, we summarize and discuss the results of the genetic studies in AAV. We also present the novel approaches to identifying the causal variants in complex susceptibility loci and disease mechanisms. Finally, we discuss the limitations of current methods and the challenges that we still have to face in order to incorporate genomic and epigenomic data into clinical practice.
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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.