Evidence map›Paper›PMID 31572400›Full record

ReviewFrontiers in immunology2019

The Era of Thromboinflammation: Platelets Are Dynamic Sensors and Effector Cells During Infectious Diseases.

Li Guo, Matthew T Rondina

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
23.1field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Plasma Proteomic Profile of Chemotherapy-Induced Severe Neutropenia: A Pilot Discovery Phase Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Platelet lipidome alterations in septic shock: a matched case-control study.Research and practice in thrombosis and haemostasis · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Observational
  20. Article

68 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

2 authors at 1 institution in 1 country.

Li GuoUniversity of Utah Molecular Medicine Program, Salt Lake City, UT, United States.
Matthew T RondinaUniversity of Utah Molecular Medicine Program, Salt Lake City, UT, United States.
University of Utah · US

Funding

New Therapies to Restore Vascular Integrity During SepsisR01HL130541 · NHLBI · UNIVERSITY OF UTAH · PI ODELBERG, SHANNON J, WEYRICH, ANDREW S · 2016 to 2020
$3.7M
Research Supplement to Impact on CMV Upon T-Cell Aging and Immune DefenseR01AG048021 · NIA · UNIVERSITY OF ARIZONA · PI NIKOLICH, JANKO Z. · 2014 to 2018
$2.6M
Translational Control of Megakaryocyte and Platelet Function in SepsisR01HL142804 · NHLBI · UNIVERSITY OF UTAH · PI RONDINA, MATTHEW THOMAS · 2018 to 2021
$1.9M
Novel Regulatory Mechanisms of Inflammation-Induced ThrombosisR56AG059877 · NIA · UNIVERSITY OF UTAH · PI RONDINA, MATTHEW THOMAS · 2018 to 2018
$381k
NHLBI NIH HHS R01 HL130541NHLBI NIH HHS R01 HL142804NIA NIH HHS R01 AG048021NIA NIH HHS R56 AG059877
6 · The paper itself

Abstract

Platelets are anucleate cells produced by megakaryocytes. In recent years, a robust body of literature supports the evolving role of platelets as key sentinel and effector cells in infectious diseases, especially critical in bridging hemostatic, inflammatory, and immune continuums. Upon intravascular pathogen invasion, platelets can directly sense viral, parasitic, and bacterial infections through pattern recognition receptors and integrin receptors or pathogen: immunoglobulin complexes through Fc and complement receptors-although our understanding of these interactions remains incomplete. Constantly scanning for areas of injury or inflammation as they circulate in the vasculature, platelets also indirectly respond to pathogen invasion through interactions with leukocytes and the endothelium. Following antigen recognition, platelets often become activated. Through a diverse repertoire of mechanisms, activated platelets can directly sequester or kill pathogens, or facilitate pathogen clearance by activating macrophages and neutrophils, promoting neutrophil extracellular traps (NETs) formation, forming platelet aggregates and microthrombi. At times, however, platelet activation may also be injurious to the host, exacerbating inflammation and promoting endothelial damage and thrombosis. There are many gaps in our understandings of the role of platelets in infectious diseases. However, with the emergence of advanced technologies, our knowledge is increasing. In the current review, we mainly discuss these evolving roles of platelets under four different infectious pathogen infections, of which are dengue, malaria,

Indexed as

AnimalsBlood PlateletsEndothelium, VascularExtracellular TrapsHumansInfectionsPlatelet AggregationThrombosisbacteriadengueinfectioninflammationmalariaplateletsepsisthromboinflammation

Identifiers

PMID31572400
PMCPMC6753373
OpenAlexW2970421739

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.