Evidence map›Paper›PMID 35254509›Full record

ReviewSeminars in immunopathology2022

Mechanisms of vascular damage in ANCA vasculitis.

David Massicotte-Azarniouch, Carolina A Herrera, J Charles Jennette, Ronald J Falk, Meghan E Free

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  11. PeerJ · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

David Massicotte-AzarniouchDivision of Nephrology and Hypertension, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.ORCID 0000-0002-6954-2030
Carolina A HerreraDivision of Nephrology and Hypertension, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.
J Charles JennetteDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Ronald J FalkDivision of Nephrology and Hypertension, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA.
Meghan E FreeDivision of Nephrology and Hypertension, Department of Medicine, University of North Carolina, Chapel Hill, NC, USA. meghan_free@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

RENAL EPIDEMIOLOGY TRAINING PROGRAMT32DK007750 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FALK, RONALD J · 1999 to 2022
$5.5M
Pathobiology of ANCA Glomerulonephritis: Targeting Adaptive and Innate Immune Processes for Precision TherapiesR01DK125350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CIAVATTA, DOMINIC J, FALK, RONALD J · 2020 to 2024
$3.4M
NIDDK NIH HHS R01 DK125350NIDDK NIH HHS T32 DK007750
6 · The paper itself

Abstract

The discovery of anti-neutrophil cytoplasmic antibodies (ANCA) and their antigenic targets, myeloperoxidase (MPO) and proteinase 3 (PR3), has led to further understanding as to the pathophysiologic processes that underlie vascular and tissue damage in ANCA vasculitis. ANCA trigger neutrophil activation leading to vascular damage in ANCA vasculitis. However, decades of study have determined that neutrophil activation alone is not sufficient to cause disease. Inflammatory stimuli are drivers of ANCA autoantigen expression and ANCA production. Certain infections or bacterial peptides may be crucial players in the initial steps of ANCA immunopathogenesis. Genetic and epigenetic alterations of gene encoding for MPO and PR3 provide additional disturbances to the immune homeostasis which provide a substrate for pathogenic ANCA formation from an adaptive immune system predisposed to autoreactivity. Promoted by inflammatory cytokines, ANCA binding leads to neutrophil activation, a process characterized by conformational changes, production and release of cytotoxic substances, and alternative complement pathway activation, thus creating an intense inflammatory milieu. This cascade of events perpetuates a vicious cycle of further inflammatory cell recruitment and activation, culminating in tissue necrosis. Our understanding of the pathogenic process in ANCA vasculitis paves the way for the development of therapies targeting crucial steps in this process. The greater appreciation of the role for complement, monocytes, and the adaptive immune system has already led to novel complement blockers and is poised to lead to further innovations which will allow for tailored antigen- or cell-specific immunotherapy targeting the autoimmune process without exposure to undue risks or toxicities.

Indexed as

Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisVasculitisAntibodies, Antineutrophil CytoplasmicAutoantigensHumansMonocytesMyeloblastinAntibodies, Antineutrophil CytoplasmicAutoantigensMyeloblastinANCA vasculitisAutoantibodyB cellGlomerulonephritisNeutrophilT cell

Identifiers

PMID35254509
PMCPMC9064952
OpenAlexW4220819727

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.