Evidence map›Paper›PMID 35686129›Full record

SynthesisFrontiers in immunology2022

Diverse Roles of NETosis in the Pathogenesis of Lupus.

Meiying Wang, Tatsuya Ishikawa, Yupeng Lai, Dhiraj Nallapothula, Ram Raj Singh

Open access · goldAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis 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 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Exercise intensity and training alter the innate immune cell type and chromosomal origins of circulating cell-free DNA in humans.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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 3 institutions in 2 countries.

Meiying WangAutoimmunity and Tolerance Laboratory, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, United States.
Tatsuya IshikawaAutoimmunity and Tolerance Laboratory, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, United States.
Yupeng LaiDepartment of Rheumatology and Immunology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Dhiraj NallapothulaAutoimmunity and Tolerance Laboratory, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, United States.
Ram Raj SinghAutoimmunity and Tolerance Laboratory, Division of Rheumatology, Department of Medicine, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, United States.
University of California, Los Angeles · USShenzhen Second People's Hospital · CNUCLA Jonsson Comprehensive Cancer Center

Funding

Gender Bias in Lupus: Contribution of Sex ChromosomesR01AR056465 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SINGH, RAM RAJ · 2008 to 2012
$2.3M
Pathogenesis of Lupus DermatitisR01AI080778 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SINGH, RAM RAJ · 2009 to 2013
$2.2M
Kidney Damage in Murine LupusR01AR050797 · NIAMS · UNIVERSITY OF CINCINNATI · PI SINGH, RAM RAJ · 2003 to 2006
$1.4M
NIAID NIH HHS R01 AI080778NIAMS NIH HHS R01 AR050797NIAMS NIH HHS R01 AR056465
6 · The paper itself

Abstract

NETosis is a form of neutrophil cell death during which extracellular fibrillary structures composed of cytosolic and granule proteins assembled on scaffolds of decondensed chromatin, called neutrophil extracellular traps (NETs), are released. NETs normally contribute to host immune defense. Accumulating evidence implicates aberrant NET production and/or reduced NET clearance, along with alterations of molecules involved in NETosis pathway, in humans and animals with lupus. The extruded nuclear antigens released by NET are a source of autoantigens, which can contribute to the breakdown of self-tolerance in lupus. Excessive NET can also promote the production of pro-inflammatory cytokine interferon-α, elicit direct cytotoxic effect on various renal cells, and cause capillary necrosis and podocyte loss. Additionally, NET can induce endothelial-to-mesenchymal transdifferentiation, which can promote activated myofibroblasts leading to extracellular matrix production. Thus, aberrant NETosis can play diverse roles, including autoantibody production, inflammation, and tissue damage, at different stages of lupus pathogenesis. Evidence suggests that treatments currently used in lupus may reduce NETosis, suggesting a potential utility of targeting NETosis to treat lupus. In fact, several approaches are being experimented to therapeutically target pathways of NETosis. Future studies should precisely delineate distinct roles of NETosis at different stages of lupus pathogenesis in humans, which would offer a rational basis for NETosis-targeting treatments in the clinic.

Indexed as

Extracellular TrapsAnimalsAutoantigensCell DeathInflammationNeutrophilsAutoantigensautoantibodyautoantigenclinical implicationsnephritisNETosispathogenesisself-tolerancesystemic lupus erythematosus

Identifiers

PMID35686129
PMCPMC9170953
OpenAlexW4285412081

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.