Evidence map›Paper›PMID 30825500›Full record

ReviewFree radical biology & medicine2019

CD36 signaling in vascular redox stress.

Moua Yang, Roy L Silverstein

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Targeting Cysteine Oxidation in Thrombotic Disorders.Antioxidants (Basel, Switzerland) · 2024
    Review
  14. Article
  15. Cysteine and methionine oxidation in thrombotic disorders.Current opinion in chemical biology · 2023
    Review
  16. Article
  17. Article
  18. NWorld journal of diabetes · 2023
    Article
  19. Review
  20. 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 2 institutions in 1 country.

Moua YangDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, WI, USA; Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI, USA.
Roy L SilversteinBlood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI, USA; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA. Electronic address: rsilverstein@mcw.edu.
Medical College of Wisconsin · USVersiti Blood Center of Wisconsin · US

Funding

ZONISMIDE IN THE TREATMENT OF SEIZURES IN PATIENTSM01RR000058 · NCRR · MEDICAL COLLEGE OF WISCONSIN · PI HYDE, JAMES F · 1985 to 2006
$19.9M
Training in Signature Transdisciplinary Cardiovascular SciencesT32HL134643 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Justin L Grobe, Jacquelyn P Kulinski · 2017 to 2026
$4.2M
ERK5 and CD36 link oxidative stress to platelet dysfunction and ischemic injuryR01HL142152 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI MORRELL, CRAIG N, SILVERSTEIN, ROY L · 2019 to 2022
$2.5M
Mechanistic Role of CD36 in ThrombosisR01HL111614 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI SILVERSTEIN, ROY L · 2013 to 2017
$1.7M
NCRR NIH HHS M01 RR000058NHLBI NIH HHS R01 HL111614NHLBI NIH HHS R01 HL142152NHLBI NIH HHS T32 HL134643
6 · The paper itself

Abstract

Scavenger receptor CD36 is a multifunctional membrane protein that promotes thrombosis in conditions of oxidative stress such as metabolic disorders including dyslipidemia, diabetes mellitus, and chronic inflammation. In these conditions, specific reactive oxidant species are generated that are context and cell dependent. In the vasculature, CD36 signaling in smooth muscle cells and endothelial cells promotes generation of reactive oxygen species, genetic downregulation of antioxidant genes, and impaired smooth muscle and endothelial function. In hematopoietic cells, CD36 signaling enhances platelet dysfunction thus decreasing the threshold for platelet activation and accelerating arterial thrombosis, whereas in macrophages, CD36 promotes lipid-laden foam cell formation and atherosclerosis. These clinically significant processes are mediated through complex redox regulated signaling mechanisms that include Src-family kinases, MAP kinases and other downstream effectors. We provide an overview of CD36 signaling in vascular redox stress highlighting the role in oxidant generation in vascular and hematopoietic cells, but with special emphasis on platelets and dyslipidemia.

Indexed as

AnimalsBlood PlateletsCD36 AntigensDyslipidemiasEndothelial CellsHumansOxidation-ReductionOxidative StressPlatelet ActivationSignal TransductionCD36 Antigens

Identifiers

PMID30825500
PMCPMC6488418
OpenAlexW2916318346

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.