Evidence map›Paper›PMID 35471483›Full record

ReviewPurinergic signalling2022

Burnstock oration - purinergic signalling in kidney transplantation.

Karen M Dwyer

Open access · hybridAbstract readReview
In one paragraph

Review in Purinergic signalling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Purinergic Signaling in Non-Parenchymal Liver Cells.International journal of molecular sciences · 2024
    Review
  2. 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

1 author at 1 institution in 1 country.

Karen M DwyerSchool of Medicine, Deakin University, Geelong, 3220, Australia. karen.dwyer@deakin.edu.au.
Deakin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney transplantation is the preferred treatment for individuals with kidney failure offering improved quality and quantity of life. Despite significant advancements in short term graft survival, longer term survival rates have not improved greatly mediated in large by chronic antibody mediated rejection. Strategies to reduce the donor kidney antigenic load may translate to improved transplant survival. CD39 on the vascular endothelium and on circulating cells, in particular regulatory T cells (Treg), is upregulated in response to hypoxic stimuli and plays a critical role in regulating the immune response removing proinflammatory ATP and generating anti-inflammatory adenosine. Herein, the role of CD39 in reducing ischaemia-reperfusion injury (IRI) and on Treg within the context of kidney transplantation is reviewed.

Indexed as

Kidney TransplantationReperfusion InjuryAdenosineAntigens, CDApyraseGraft SurvivalHumansKidneySignal TransductionAdenosineAntigens, CDApyraseAdenosine receptorsATPCD39Ischaemia reperfusion injuryRegulatory T cellsTreg

Identifiers

PMID35471483
PMCPMC9832191
OpenAlexW4224443413

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.