Evidence map›Paper›PMID 31010696›Full record

ReviewHuman immunology2019

Antibodies against Angiotensin II Type 1 and Endothelin A Receptors: Relevance and pathogenicity.

Mary Carmelle Philogene, Tory Johnson, Arthur Jason Vaught, Sammy Zakaria, Neal Fedarko

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Human immunology, 2019. 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
7.5field-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

42 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. Observational
  13. Review
  14. Angiotensin II Type-1 Receptor Antibody in Solid Organ Transplantation - Is It Time to Test?Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
  15. Editorial: Antibody-mediated rejection.Frontiers in transplantation · 2024
    Article
  16. Article
  17. Review
  18. 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

5 authors at 2 institutions in 1 country.

Mary Carmelle PhilogeneDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States. Electronic address: mphilogene@jhmi.edu.
Tory JohnsonDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Arthur Jason VaughtDepartment of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Sammy ZakariaDepartment of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Neal FedarkoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

The Johns Hopkins Clinical Research Scholars in Women's Health (BIRCWH)K12HD085845 · NICHD · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2015 to 2023
$4.5M
NICHD NIH HHS K12 HD085845
6 · The paper itself

Abstract

Antibodies against two G-protein coupled receptors (GPCRs), angiotensin II type 1 receptor (AT1R) and endothelin A receptor (ETAR) are among a growing number of autoantibodies that are found to be associated with allograft dysfunction. AT1R antibodies (AT1Rabs) and ETAR antibodies (ETARabs) have been shown to activate their target receptors and affect signaling pathways. Multiple single center reports have shown an association between presence of these antibodies and acute or chronic rejection and graft loss in kidney, heart, liver, lung and composite tissue transplantations. However, the characteristics of patients that are most likely to develop adverse outcomes, the phenotypes associated with graft damage solely due to these antibodies, and the antibody titer required to cause dysfunction are areas that remain controversial. This review compiles existing knowledge on the effect of antibodies against GPCRs in other diseases in order to bridge the gap in knowledge within transplantation biology. Future areas for research are highlighted and include the need for functional assays and treatment protocols for transplant patients who present with AT1Rabs and ETARabs. Understanding how antibodies that activate GPCRs influence transplantation outcome will have direct clinical implications for preemptive evaluation of transplant candidates as well as the post-transplant care of organ recipients.

Indexed as

Organ TransplantationAnimalsAutoantibodiesGraft RejectionHumansPhenotypeReceptor, Angiotensin, Type 1Receptor, Endothelin ASignal TransductionTransplantation ImmunologyAutoantibodiesReceptor, Angiotensin, Type 1Receptor, Endothelin AAllograft dysfunctionAngiotensin II type 1 receptor antibodyEndothelin A receptor antibodyNon-HLA antibodies

Identifiers

PMID31010696
PMCPMC8015780
OpenAlexW2938095270

What Socratic 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 Socratic graph.