Evidence map›Paper›PMID 31416173›Full record

ReviewBiomolecules2019

Neutrophil Extracellular Trap Formation: Physiology, Pathology, and Pharmacology.

Mithunan Ravindran, Meraj A Khan, Nades Palaniyar

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed, 2 pooled it
8.7field-weighted citation impact, top 2% 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

211 citing papers in PubMed, 2 syntheses or guidelines pooled it, 304 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Science advances · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Neutrophil extracellular traps (NETosis) in gynecologic cancers: from pathogenesis to therapeutic opportunities: a narrative review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

151 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Mithunan RavindranProgram in Translational Medicine, SickKids Research Institute, The Hospital for Sick Children, Toronto, ON M5G1X8, Canada.
Meraj A KhanProgram in Translational Medicine, SickKids Research Institute, The Hospital for Sick Children, Toronto, ON M5G1X8, Canada.
Nades PalaniyarProgram in Translational Medicine, SickKids Research Institute, The Hospital for Sick Children, Toronto, ON M5G1X8, Canada. nades.palaniyar@sickkids.ca.ORCID 0000-0002-2170-8548
University of Toronto · CA

Funding

CIHR MOP-111012
6 · The paper itself

Abstract

Neutrophil extracellular traps (NETs), a unique DNA framework decorated with antimicrobial peptides, have been in the scientific limelight for their role in a variety of pathologies ranging from cystic fibrosis to cancer. The formation of NETs, as well as relevant regulatory mechanisms, physiological factors, and pharmacological agents have not been systematically discussed in the context of their beneficial and pathological aspects. Novel forms of NET formation including vital NET formation continue to be uncovered, however, there remain fundamental questions around established mechanisms such as NADPH-oxidase (Nox)-dependent and Nox-independent NET formation. Whether NET formation takes place in the tissue versus the bloodstream, internal factors (e.g. reactive oxygen species (ROS) production and transcription factor activation), and external factors (e.g. alkaline pH and hypertonic conditions), have all been demonstrated to influence specific NET pathways. Elements of neutrophil biology such as transcription and mitochondria, which were previously of unknown significance, have been identified as critical mediators of NET formation through facilitating chromatin decondensation and generating ROS, respectively. While promising therapeutics inhibiting ROS, transcription, and gasdermin D are being investigated, neutrophil phagocytosis plays a critical role in host defense and any therapies targeting NET formation must avoid impairing the physiological functions of these cells. This review summarizes what is known in the many domains of NET research, highlights the most relevant challenges in the field, and inspires new questions that can bring us closer to a unified model of NET formation.

Indexed as

AnimalsExtracellular TrapsHumansNeutrophilsReactive Oxygen SpeciesReactive Oxygen Speciesautoimmunitycancer metastasiscystic fibrosisdiabetesNeutrophil extracellular trapsNox-dependent/Nox-independent/suicidal/vital NETs

Identifiers

PMID31416173
PMCPMC6722781
OpenAlexW2969016415

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.