Evidence map›Paper›PMID 26136559›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Interactions between HIF-1α and AMPK in the regulation of cellular hypoxia adaptation in chronic kidney disease.

Hui Li, Joseph Satriano, Joanna L Thomas, Satoshi Miyamoto, Kumar Sharma, Núria M Pastor-Soler, Kenneth R Hallows, Prabhleen Singh

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article 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. It is linked to trial NCT06654921 (The Safety and Efficacy of Remote Ischemic Conditioning for the Treatment of Diabetic Kidney Disease), which is not on this map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% 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.

NCT06654921 nanot yet recruitingnot on this mapstarted 2025, after this paper: background citation

The Safety and Efficacy of Remote Ischemic Conditioning for the Treatment of Diabetic Kidney Disease: a Single-center Double-blinded Randomized Controlled Study

TypeinterventionalSponsorCapital Medical UniversityRan2025 to 2025Enrolled60ConditionsDiabetic Kidney Disease (DKD)ArmsRemote ischemic conditioning, Sham remote ischemic conditioning, Standard medication therapy
3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Kidney Energetics and Cyst Burden in Autosomal Dominant Polycystic Kidney Disease: A Pilot Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
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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

8 authors at 2 institutions in 1 country.

Hui LiDepartment of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;
Joseph SatrianoDivision of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and.
Joanna L ThomasDivision of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and.
Satoshi MiyamotoDivision of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and Center for Renal Translational Medicine, University of California, San Diego, California.
Kumar SharmaDivision of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and Center for Renal Translational Medicine, University of California, San Diego, California.
Núria M Pastor-SolerDepartment of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;
Kenneth R HallowsDepartment of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California;
Prabhleen SinghDivision of Nephrology and Hypertension, Department of Medicine, University of California and Veterans Affairs San Diego Healthcare System, San Diego, California; and p1singh@ucsd.edu.
VA San Diego Healthcare System · USUniversity of Southern California · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
Mechanisms and Relevance of Sodium Transport Regulation by AMPKR01DK075048 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HALLOWS, KENNETH R · 2007 to 2015
$2.5M
Mechanisms of Kinase-dependent Regulation of the V-ATPase in KidneyR01DK084184 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PASTOR-SOLER, NURIA M. · 2009 to 2013
$1.5M
Pathophysiology of Early Chronic Kidney Disease: Response to Ischemia-ReperfusionK08DK084305 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SINGH, PRABHLEEN · 2010 to 2014
$760k
Renal Oxygenation in the Pathophysiology of Kidney DiseaseI01BX002175 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI SINGH, PRABHLEEN · 2015 to 2025
–
BLRD VA I01 BX002175NIDDK NIH HHS K08 DK084305NIDDK NIH HHS K08-DK-084305NIDDK NIH HHS P30 DK079307NIDDK NIH HHS P30-DK-079307NIDDK NIH HHS P30 DK079337NIDDK NIH HHS P30-DK-079337NIDDK NIH HHS R01 DK075048NIDDK NIH HHS R01-DK-075048NIDDK NIH HHS R01-DK-84184
6 · The paper itself

Abstract

Renal hypoxia contributes to chronic kidney disease (CKD) progression, as validated in experimental and human CKD. In the early stages, increased oxygen consumption causes oxygen demand/supply mismatch, leading to hypoxia. Hence, early targeting of the determinants and regulators of oxygen consumption in CKD may alter the disease course before permanent damage ensues. Here, we focus on hypoxia inducible factor-1α (HIF-1α) and AMP-activated protein kinase (AMPK) and on the mechanisms by which they may facilitate cellular hypoxia adaptation. We found that HIF-1α activation in the subtotal nephrectomy (STN) model of CKD limits protein synthesis, inhibits apoptosis, and activates autophagy, presumably for improved cell survival. AMPK activation was diminished in the STN kidney and was remarkably restored by HIF-1α activation, demonstrating a novel role for HIF-1α in the regulation of AMPK activity. We also investigated the independent and combined effects of HIF-1α and AMPK on cell survival and death pathways by utilizing pharmacological and knockdown approaches in cell culture models. We found that the effect of HIF-1α activation on autophagy is independent of AMPK, but on apoptosis it is partially AMPK dependent. The effects of HIF-1α and AMPK activation on inhibiting protein synthesis via the mTOR pathway appear to be additive. These various effects were also observed under hypoxic conditions. In conclusion, HIF-1α and AMPK appear to be linked at a molecular level and may act as components of a concerted cellular response to hypoxic stress in the pathophysiology of CKD.

Indexed as

Adaptation, PhysiologicalAMP-Activated Protein KinasesAnimalsApoptosisAutophagyCell HypoxiaDisease Models, AnimalHypoxia-Inducible Factor 1, alpha SubunitMaleNephrectomyRatsRats, WistarRenal CirculationRenal Insufficiency, ChronicTOR Serine-Threonine KinasesAMP-Activated Protein KinasesHypoxia-Inducible Factor 1, alpha SubunitmTOR protein, ratTOR Serine-Threonine KinasesAMP-activated protein kinasehypoxia inducible factor-1α

Identifiers

PMID26136559
PMCPMC4556888
OpenAlexW2174122845

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.