Evidence map›Paper›PMID 35861953›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2022

Thromboinflammation: From Atherosclerosis to COVID-19.

Denisa D Wagner, Lukas A Heger

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.0field-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

47 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. LPCAT3-dependent remodeling of the phospholipids and lipid rafts is essential for vascular proinflammatory signaling and the development of atherosclerosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Thromboinflammatory complications ofFrontiers in immunology · 2025
    Review
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

2 authors at 1 institution in 1 country.

Denisa D WagnerProgram in Cellular and Molecular Medicine, Division of Hematology and Oncology, Boston Children's Hospital/Harvard Medical School, MA (D.D.W., L.A.H.).ORCID 0000-0002-4494-413X
Lukas A HegerProgram in Cellular and Molecular Medicine, Division of Hematology and Oncology, Boston Children's Hospital/Harvard Medical School, MA (D.D.W., L.A.H.).ORCID 0000-0002-9419-5675
Boston Children's Hospital · US

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

The activating interplay of thrombosis and inflammation (thromboinflammation) has been established as a major underlying pathway, driving not only cardiovascular disease but also autoimmune disease and most recently, COVID-19. Throughout the years, innate immune cells have emerged as important modulators of this process. As the most abundant white blood cell in humans, neutrophils are well-positioned to propel thromboinflammation. This includes their ability to trigger an organized cell death pathway with the release of decondensed chromatin structures called neutrophil extracellular traps. Decorated with histones and cytoplasmic and granular proteins, neutrophil extracellular traps exert cytotoxic, immunogenic, and prothrombotic effects accelerating disease progression. Distinct steps leading to extracellular DNA release (NETosis) require the activities of PAD4 (protein arginine deiminase 4) catalyzing citrullination of histones and are supported by neutrophil inflammasome. By linking the immunologic function of neutrophils with the procoagulant and proinflammatory activities of monocytes and platelets, PAD4 activity holds important implications for understanding the processes that fuel thromboinflammation. We will also discuss mechanisms whereby vascular occlusion in thromboinflammation depends on the interaction of neutrophil extracellular traps with ultra-large VWF (von Willebrand Factor) and speculate on the importance of PAD4 in neutrophil inflammasome assembly and neutrophil extracellular traps in thromboinflammatory diseases including atherosclerosis and COVID-19.

Indexed as

AtherosclerosisCOVID-19Extracellular TrapsThrombosisHistonesHumansInflammasomesInflammationNeutrophilsThromboinflammationvon Willebrand FactorHistonesInflammasomesvon Willebrand FactoratheroschlerosisCOVID-19histonesinflammasomesneutrophilsplateletsprotein arginine deiminase type 4

Identifiers

PMID35861953
PMCPMC9420806
OpenAlexW4284959148

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.