Evidence map›Paper›PMID 25287331›Full record

ReviewActa physiologica (Oxford, England)2015

Adenosine receptors and renal ischaemia reperfusion injury.

M M Rabadi, H T Lee

Open access · greenAbstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Role of G protein coupled receptors in acute kidney injury.Cell communication and signaling : CCS · 2024
    Review
  6. Article
  7. Renoprotective strategies.World journal of nephrology · 2024
    Article
  8. Article
  9. Article
  10. Regionally selective cardiovascular responses to adenosine AFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  11. Review
  12. The adenosine pathway in immuno-oncology.Nature reviews. Clinical oncology · 2020
    Review
  13. Role of Cardiac AFrontiers in pharmacology · 2020
    Review
  14. Perivascular CD73American journal of physiology. Renal physiology · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

M M RabadiDepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA.
H T Lee
Columbia University · US

Funding

Renal Protection With A1 Adenosine ReceptorsR01DK058547 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, H. THOMAS · 2001 to 2015
$4.6M
Mechanisms of Renal Protection with Volatile AnestheticsR01GM067081 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, H. THOMAS · 2004 to 2015
$4.0M
NIDDK NIH HHS DK-058547NIDDK NIH HHS R01 DK058547NIGMS NIH HHS GM-067081NIGMS NIH HHS R01 GM067081
6 · The paper itself

Abstract

One of the frequent clinical complications that results in billions of dollars in healthcare costs annually in the United States is acute kidney injury (AKI). Ischaemia reperfusion (IR) injury is a major cause AKI. Unfortunately, no effective treatment or preventive measure for AKI exists. With increased surgical complexity coupled with increasing number of elderly, the incidence of AKI is becoming more frequent. Adenosine is a metabolic breakdown product of adenosine triphosphate (ATP) and contributes to the regulation of multiple physiological events. Extracellular adenosine activates four subtypes of adenosine receptors (AR) including A1 AR, A2 A AR, A2 B AR and A3 AR. In the kidney, adenosine regulates glomerular filtration rate, vascular tone, renin release and is an integrative part of tubular glomerular feedback signal to the afferent arterioles. In addition, each AR subtype powerfully modulates renal IR injury. The A1 AR activation protects against ischaemic insult by reducing apoptosis, necrosis and inflammation. Activation of A2 A AR protects against renal injury by modulating leucocyte-mediated inflammation as well as directly reducing renal tubular inflammation. Activation of A2 B AR acts via direct activation of renal parenchymal as well as renovascular receptors and is important in kidney preconditioning. Finally, activation of A3 AR exacerbates renal damage following renal IR injury while A3 AR antagonism attenuates renal damage following ischaemic insult. Latest body of research suggests that kidney AR modulation may be a promising approach to treat ischaemic AKI. This brief review focuses on the signalling pathways of adenosine in the kidney followed by the role for various AR modulations in protecting against ischaemic AKI.

Indexed as

AnimalsApoptosisHumansKidney DiseasesNecrosisReceptors, Purinergic P1Reperfusion InjuryReceptors, Purinergic P1acute kidney injuryacute renal failureapoptosisinflammationnecrosis

Identifiers

PMID25287331
PMCPMC4270901
OpenAlexW2081493694

What OpenQuestion holds

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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.