Evidence map›Paper›PMID 24025642›Full record

ArticleKidney international2014

Selective deletion of the endothelial sphingosine-1-phosphate 1 receptor exacerbates kidney ischemia-reperfusion injury.

Ahrom Ham, Mihwa Kim, Joo Yun Kim, Kevin M Brown, Marcus Fruttiger, Vivette D D'Agati, H Thomas Lee

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

Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
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  11. Review
  12. Piezo1 mediates angiogenesis through activation of MT1-MMP signaling.American journal of physiology. Cell physiology · 2019
    Article
  13. Sphingosine 1-phosphate receptor subtype 3 (S1PJournal of neuroinflammation · 2018
    Article
  14. TGF-β/Smad3 pathway enhances the cardio-protection of S1R/SIPR1 inExperimental and therapeutic medicine · 2018
    Article
  15. Article
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  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Ahrom HamDepartment of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia University, Columbia University, New York, New York, USA.
Mihwa KimDepartment of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia University, Columbia University, New York, New York, USA.
Joo Yun KimDepartment of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia University, Columbia University, New York, New York, USA.
Kevin M BrownDepartment of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia University, Columbia University, New York, New York, USA.
Marcus FruttigerUCL Institute of Ophthalmology, University College London, London, UK.
Vivette D D'AgatiDepartment of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York, USA.
H Thomas LeeDepartment of Anesthesiology, Anesthesiology Research Laboratories, College of Physicians and Surgeons of Columbia University, Columbia University, New York, New York, USA.
Columbia University · USUniversity College London · GB

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
Medical Research Council G0501711NIDDK NIH HHS R01 DK-058547NIDDK NIH HHS R01 DK058547NIGMS NIH HHS R01 GM-067081NIGMS NIH HHS R01 GM067081
6 · The paper itself

Abstract

The role for the endothelial sphingosine-1-phosphate 1 receptor (S1P1R) in acute kidney injury (AKI) remains unclear as germline endothelial S1P1R deletion is embryonically lethal. Here, we generated conditional endothelial S1P1R deficiency by crossing mice with floxed S1P1R with mice expressing a tamoxifen-inducible form of Cre recombinase under the transcriptional control of the platelet-derived growth factor-β (Pdgfβ) gene. Mice with tamoxifen-induced deletion of endothelial S1P1R had increased renal tubular necrosis, inflammation, and impaired vascular permeability, as well as exacerbated renal tubular apoptosis after ischemic AKI compared with tamoxifen-treated wild-type mice. Moreover, endothelial S1P1R deletion resulted in increased hepatic injury after ischemic AKI. As a potential mechanism for exacerbated renal injury, conditional endothelial S1P1R-null mice had markedly reduced endothelial HSP27 expression compared with wild-type mice. Cultured glomerular endothelial cells treated with a specific S1P1R antagonist (W146) for 3 days also showed reduced HSP27 expression compared with vehicle-treated cells. Finally, mice treated with W146 for 3 days also showed reduced endothelial HSP27 expression as well as exacerbated renal and hepatic injury after ischemic AKI. Thus, our studies demonstrate a protective role for endothelial S1P1R against ischemic AKI most likely by regulating endothelial barrier integrity and endothelial HSP27 expression.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCapillary PermeabilityEndothelial CellsEndotheliumGene ExpressionGene Knockdown TechniquesHSP27 Heat-Shock ProteinsKidneyLiverLiver DiseasesMaleMiceMice, Inbred C57BLMice, TransgenicHSP27 Heat-Shock ProteinsHspb2 protein, mouseReceptors, Lysosphingolipid

Identifiers

PMID24025642
PMCPMC3952061
OpenAlexW2030866548

What OpenQuestion 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 OpenQuestion graph.