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Equilibrative nucleoside transporter 1 (ENT1) regulates postischemic blood flow during acute kidney injury in mice

2012· article· en· 106 citations· W2145142784 on OpenAlex· 10.1172/jci60214

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.

Post-publication record

Nature
Retraction
Reason
Duplication of/in Image;Falsification/Fabrication of Data;Investigation by Company/Institution;Investigation by Journal/Publisher;Misconduct - Official Investigation(s) and/or Finding(s);Misconduct by Author;Unreliable Results and/or Conclusions;Upgrade/Update of Prior Notice(s);
Date
6/1/2017 0:00
Flagged by OpenAlex?
Yes

Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.

Abstract

A complex biologic network regulates kidney perfusion under physiologic conditions. This system is profoundly perturbed following renal ischemia, a leading cause of acute kidney injury (AKI) - a life-threatening condition that frequently complicates the care of hospitalized patients. Therapeutic approaches to prevent and treat AKI are extremely limited. Better understanding of the molecular pathways promoting postischemic reflow could provide new candidate targets for AKI therapeutics. Due to its role in adapting tissues to hypoxia, we hypothesized that extracellular adenosine has a regulatory function in the postischemic control of renal perfusion. Consistent with the notion that equilibrative nucleoside transporters (ENTs) terminate adenosine signaling, we observed that pharmacologic ENT inhibition in mice elevated renal adenosine levels and dampened AKI. Deletion of the ENTs resulted in selective protection in Ent1-/- mice. Comprehensive examination of adenosine receptor-knockout mice exposed to AKI demonstrated that renal protection by ENT inhibitors involves the A2B adenosine receptor. Indeed, crosstalk between renal Ent1 and Adora2b expressed on vascular endothelia effectively prevented a postischemic no-reflow phenomenon. These studies identify ENT1 and adenosine receptors as key to the process of reestablishing renal perfusion following ischemic AKI. If translatable from mice to humans, these data have important therapeutic implications.

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The record

Venue
Journal of Clinical Investigation
Topic
Adenosine and Purinergic Signaling
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
York University
Funders
National Institute of Diabetes and Digestive and Kidney DiseasesNational Heart, Lung, and Blood InstituteUniversity of Colorado DenverNational Cancer InstituteNational Institutes of HealthCrohn's and Colitis FoundationCrohn's and Colitis Foundation of AmericaDeutsche ForschungsgemeinschaftNational Center for Research ResourcesAmerican Heart Association
Keywords
NucleosideAcute kidney injuryBlood flowKidneyMedicineRenal blood flowTransporterPharmacologyCardiologyInternal medicineChemistryGeneBiochemistry
Has abstract in OpenAlex
yes