Evidence map›Paper›PMID 25593280›Full record

ReviewCirculation research2015

Fcγ receptors and ligands and cardiovascular disease.

Keiji Tanigaki, Nathan Sundgren, Amit Khera, Wanpen Vongpatanasin, Chieko Mineo, Philip W Shaul

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Observational
  3. Review
  4. Article
  5. Article
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  7. Epigenomics and transcriptomics association study of blood pressure and incident diagnosis of hypertension in twins.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  8. Article
  9. Review
  10. Modified human mesenchymal stromal/stem cells restore cortical excitability after focal ischemic stroke in rats.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Biomedicines · 2022
    Article
  20. Article
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

6 authors at 1 institution in 1 country.

Keiji TanigakiFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas.
Nathan SundgrenFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas.
Amit KheraFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas.
Wanpen VongpatanasinFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas.
Chieko MineoFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas.
Philip W ShaulFrom the Department of Pediatrics, Center for Pulmonary and Vascular Biology (K.T., N.S., C.M., P.W.S.), and Division of Cardiology, Department of Internal Medicine (A.K., W.V.), University of Texas Southwestern Medical Center, Dallas. philip.shaul@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

Fc gamma RIIB and Inflammation-Related Vascular DiseaseR01HL115122 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAUL, PHILIP W · 2013 to 2016
$1.4M
NHLBI NIH HHS HL115122NHLBI NIH HHS R01 HL115122
6 · The paper itself

Abstract

Fcγ receptors (FcγRs) classically modulate intracellular signaling on binding of the Fc region of IgG in immune response cells. How FcγR and their ligands affect cardiovascular health and disease has been interrogated recently in both preclinical and clinical studies. The stimulation of activating FcγR in endothelial cells, vascular smooth muscle cells, and monocytes/macrophages causes a variety of cellular responses that may contribute to vascular disease pathogenesis. Stimulation of the lone inhibitory FγcR, FcγRIIB, also has adverse consequences in endothelial cells, antagonizing NO production and reparative mechanisms. In preclinical disease models, activating FcγRs promote atherosclerosis, whereas FcγRIIB is protective, and activating FcγRs also enhance thrombotic and nonthrombotic vascular occlusion. The FcγR ligand C-reactive protein (CRP) has undergone intense study. Although in rodents CRP does not affect atherosclerosis, it causes hypertension and insulin resistance and worsens myocardial infarction. Massive data have accumulated indicating an association between increases in circulating CRP and coronary heart disease in humans. However, Mendelian randomization studies reveal that CRP is not likely a disease mediator. CRP genetics and hypertension warrant further investigation. To date, studies of genetic variants of activating FcγRs are insufficient to implicate the receptors in coronary heart disease pathogenesis in humans. However, a link between FcγRIIB and human hypertension may be emerging. Further knowledge of the vascular biology of FcγR and their ligands will potentially enhance our understanding of cardiovascular disorders, particularly in patients whose greater predisposition for disease is not explained by traditional risk factors, such as individuals with autoimmune disorders.

Indexed as

AnimalsCardiovascular DiseasesC-Reactive ProteinHumansImmunity, CellularLigandsReceptors, IgGSignal TransductionC-Reactive ProteinLigandsReceptors, IgGatherosclerosisC-reactive proteinhypertensionnitric oxide synthase type III

Identifiers

PMID25593280
PMCPMC4331353
OpenAlexW2133841841

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.