Evidence map›Paper›PMID 20308331›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2010

Protection against acute kidney injury via A(1) adenosine receptor-mediated Akt activation reduces liver injury after liver ischemia and reperfusion in mice.

Sang Won Park, Sean W C Chen, Mihwa Kim, Kevin M Brown, Vivette D D'Agati, H Thomas Lee

Abstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Review
  2. Caffeine and neonatal acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2024
    Review
  3. Article
  4. Article
  5. Improving Molecular Therapy in the Kidney.Molecular diagnosis & therapy · 2020
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Volatile anesthetics and AKI: risks, mechanisms, and a potential therapeutic window.Journal of the American Society of Nephrology : JASN · 2014
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Global consequences of liver ischemia/reperfusion injury.Oxidative medicine and cellular longevity · 2014
    Review
  17. Updates on Hepato-Renal Syndrome.Journal of anesthesia & clinical research · 2013
    Article
  18. Article
  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

6 authors.

Sang Won ParkDepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, New York 10032-3784, USA.
Sean W C Chen
Mihwa Kim
Kevin M Brown
Vivette D D'Agati
H Thomas Lee

Funding

Renal Protection With A1 Adenosine ReceptorsR01DK058547 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, H. THOMAS · 2001 to 2015
$4.6M
NIDDK NIH HHS DK58547NIDDK NIH HHS R01 DK058547
6 · The paper itself

Abstract

Hepatic ischemia reperfusion (IR) injury causes acute kidney injury (AKI). However, the contribution of AKI to the pathogenesis of liver IR injury is unclear. Furthermore, controversy still exists regarding the role of A(1) adenosine receptors (A(1)ARs) in AKI. In this study, we determined whether exogenous and endogenous A(1)AR activation protects against AKI with subsequent liver protection after hepatic IR in mice. We found that after hepatic IR A(1) knockout (KO) mice and A(1)AR antagonist-treated A(1) wild-type (WT) mice developed worse AKI and liver injury compared with vehicle-treated A(1)WT mice. Moreover, a selective A(1)AR agonist protected against hepatic IR-induced AKI and liver injury in A(1)WT mice. Renal A(1)AR-mediated kidney protection plays a crucial role in protecting the liver after IR because: 1) selective unilateral renal lentiviral overexpression of human A(1)ARs [enhanced green fluorescent protein (EGFP)-huA(1)AR] in A(1)KO mice protected against both kidney and liver injury sustained after liver IR, 2) removal of the EGFP-huA(1)AR lentivirus-injected kidney from A(1)KO mice abolished both renal and hepatic protection after liver IR, and 3) bilateral nephrectomy before hepatic ischemia abolished the protective effects of A(1)AR activation in A(1)WT mice. Finally, inhibition of Akt, but not extracellular signal-regulated kinase mitogen-activated protein kinase, prevented the kidney and liver protection afforded by A(1)AR agonist treatment. Taken together, we show that endogenous and exogenous activation of renal A(1)ARs protect against liver and kidney injury after liver IR in vivo via pathways involving Akt activation.

Indexed as

ActinsAcute Kidney InjuryAlanine TransaminaseAnimalsApoptosisCapillary PermeabilityCreatinineEnzyme-Linked Immunosorbent AssayHumansInterleukin-6KidneyLentivirusLiverLiver DiseasesMiceMice, KnockoutActinsAlanine TransaminaseCreatinineInterleukin-6Oncogene Protein v-aktReceptor, Adenosine A1RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID20308331
PMCPMC2879934

What OpenQuestion holds

Textmetadata
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.