Evidence map›Paper›PMID 26311114›Full record

ReviewAmerican journal of physiology. Renal physiology2015

Molecular mechanisms of ischemic preconditioning in the kidney.

Pinelopi P Kapitsinou, Volker H Haase

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Observational
  3. Review
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  5. Article
  6. Review
  7. Article
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  10. PGC1Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Ischemic Preconditioning of the Kidney.Bulletin of experimental biology and medicine · 2021
    Review
  18. Article
  19. Review
  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 2 institutions in 1 country.

Pinelopi P KapitsinouDepartments of Medicine, Anatomy and Cell Biology, and the Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas; pkapitsinou@kumc.edu.
Volker H HaaseDepartments of Medicine, Cancer Biology, and Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee; and Medicine and Research Services, Department of Veterans Affairs Hospital, Tennessee Valley Healthcare System, Nashville, Tennessee.ORCID http://orcid.org/0000-0002-7051-8994
University of Kansas Medical Center · USVanderbilt University · US

Funding

Transgenic and Gener-Targeting CoreP20GM104936 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SAADI, IRFAN · 2012 to 2016
$10.9M
Molecular Mechanisms of Renal InjuryR01DK081646 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HAASE, VOLKER HANS · 2008 to 2021
$4.3M
Metabolic Reprogramming in Acute Kidney InjuryR01DK101791 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HAASE, VOLKER HANS · 2014 to 2018
$1.8M
Hypoxia-Inducible Factors in Liver MetabolismR01DK080821 · NIDDK · VANDERBILT UNIVERSITY · PI HAASE, VOLKER HANS · 2009 to 2013
$1.7M
Cellular and Molecular Mechanisms of Renal AnemiaI01BX002348 · VA · VETERANS HEALTH ADMINISTRATION · PI Volker Hans Haase · 2014 to 2026
–
NIDDK NIH HHS R01 DK080821NIDDK NIH HHS R01-DK080821NIDDK NIH HHS R01 DK081646NIDDK NIH HHS R01-DK081646NIDDK NIH HHS R01 DK101791NIDDK NIH HHS R01-DK101791NIGMS NIH HHS P20 GM104936
6 · The paper itself

Abstract

More effective therapeutic strategies for the prevention and treatment of acute kidney injury (AKI) are needed to improve the high morbidity and mortality associated with this frequently encountered clinical condition. Ischemic and/or hypoxic preconditioning attenuates susceptibility to ischemic injury, which results from both oxygen and nutrient deprivation and accounts for most cases of AKI. While multiple signaling pathways have been implicated in renoprotection, this review will focus on oxygen-regulated cellular and molecular responses that enhance the kidney's tolerance to ischemia and promote renal repair. Central mediators of cellular adaptation to hypoxia are hypoxia-inducible factors (HIFs). HIFs play a crucial role in ischemic/hypoxic preconditioning through the reprogramming of cellular energy metabolism, and by coordinating adenosine and nitric oxide signaling with antiapoptotic, oxidative stress, and immune responses. The therapeutic potential of HIF activation for the treatment and prevention of ischemic injuries will be critically examined in this review.

Indexed as

Ischemic PreconditioningAcute Kidney InjuryAnimalsHumansHypoxiaHypoxia-Inducible Factor 1KidneyOxidative StressHypoxia-Inducible Factor 1acute kidney injuryadenosinedioxygenaseserythropoietinHIF prolyl-4-hydroxylaseshypoxiahypoxia-inducible factorinflammationischemic preconditioningoxygen sensing

Identifiers

PMID26311114
PMCPMC4652073
OpenAlexW2097697450

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.