Evidence map›Paper›PMID 31518165›Full record

ReviewCirculation research2019

Extracellular DNA NET-Works With Dire Consequences for Health.

Nicoletta Sorvillo, Deya Cherpokova, Kimberly Martinod, Denisa D Wagner

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
7.4field-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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Neutrophil death-more than meets the eye.Experimental hematology · 2025
    Review
  18. Article
  19. Review
  20. Article

63 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

4 authors at 3 institutions in 2 countries.

Nicoletta SorvilloFrom the Program in Cellular and Molecular Medicine (N.S., D.C., D.D.W.), Boston Children's Hospital, MA.
Deya CherpokovaFrom the Program in Cellular and Molecular Medicine (N.S., D.C., D.D.W.), Boston Children's Hospital, MA.
Kimberly MartinodLaboratory for Thrombosis Research, KU Leuven Campus Kulak Kortrijk, Belgium (K.M.).
Denisa D WagnerFrom the Program in Cellular and Molecular Medicine (N.S., D.C., D.D.W.), Boston Children's Hospital, MA.
Harvard University · USBoston Children's Hospital · USKU Leuven · BE

Funding

How inflammation and thrombosis fuel disease and aging: Focus on NETsR35HL135765 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI WAGNER, DENISA D · 2017 to 2023
$6.2M
NHLBI NIH HHS R35 HL135765
6 · The paper itself

Abstract

Neutrophils play a central role in innate immune defense. Advances in neutrophil biology have brought to light the capacity of neutrophils to release their decondensed chromatin and form large extracellular DNA networks called neutrophil extracellular traps (NETs). NETs are produced in response to many infectious and noninfectious stimuli and, together with fibrin, block the invasion of pathogens. However, their formation in inflamed blood vessels produces a scaffold that supports thrombosis, generates neo-antigens favoring autoimmunity, and aggravates damage in ischemia/reperfusion injury. NET formation can also be induced by cancer and promotes tumor progression. Formation of NETs within organs can be immediately detrimental, such as in lung alveoli, where they affect respiration, or they can be harmful over longer periods of time. For example, NETs initiate excessive deposition of collagen, resulting in fibrosis, thus likely contributing to heart failure. Here, we summarize the latest knowledge on NET generation and discuss how excessive NET formation mediates propagation of thrombosis and inflammation and, thereby, contributes to various diseases. There are many ways in which NET formation could be averted or NETs neutralized to prevent their detrimental consequences, and we will provide an overview of these possibilities.

Indexed as

AnimalsAtherosclerosisAutoimmune DiseasesExtracellular TrapsHumansLung DiseasesMetabolomeThrombosisautoimmunitycardiovascular diseasefibrosisinflammationneutrophils

Identifiers

PMID31518165
PMCPMC6746252
OpenAlexW2965111812

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.