Evidence map›Paper›PMID 24990892›Full record

ArticleAmerican journal of physiology. Renal physiology2014

Renal cortical hexokinase and pentose phosphate pathway activation through the EGFR/Akt signaling pathway in endotoxin-induced acute kidney injury.

Joshua A Smith, L Jay Stallons, Rick G Schnellmann

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

55 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Lactate metabolism and acute kidney injury.Chinese medical journal · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Gut microbiota and neonatal acute kidney injury biomarkers.Pediatric nephrology (Berlin, Germany) · 2023
    Review
  17. Review
  18. Review
  19. Review
  20. Vitamin D-Frontiers in physiology · 2023
    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

3 authors at 2 institutions in 1 country.

Joshua A SmithDepartment of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina; and.
L Jay StallonsDepartment of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina; and.
Rick G SchnellmannDepartment of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina; and Ralph H. Johnson Veterans Administration Medical Center, Charleston, South Carolina schnell@musc.edu.
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · US

Funding

SOUTH CAROLINA COBRE IN OXIDANTS, REDOX BALANCE AND STRESS SIGNALINGP20GM103542 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TEW, KENNETH D. · 2012 to 2020
$20.2M
SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
Mitochondrial Biogenesis Promotes Recovery From Oxidant InjuryR01GM084147 · NIGMS · UNIVERSITY OF ARIZONA · PI SCHNELLMANN, RICK G · 2008 to 2016
$2.4M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CROUCH, ROSALIE K · 2002 to 2002
$2.0M
NCRR NIH HHS C06-RR015455NCRR NIH HHS UL1 RR029882NCRR NIH HHS UL1-RR029882NIGMS NIH HHS GM084147NIGMS NIH HHS P20GM103542-02NIGMS NIH HHS R01 GM084147
6 · The paper itself

Abstract

While disruption of energy production is an important contributor to renal injury, metabolic alterations in sepsis-induced AKI remain understudied. We assessed changes in renal cortical glycolytic metabolism in a mouse model of sepsis-induced AKI. A specific and rapid increase in hexokinase (HK) activity (∼2-fold) was observed 3 h after LPS exposure and maintained up to 18 h, in association with a decline in renal function as measured by blood urea nitrogen (BUN). LPS-induced HK activation occurred independently of HK isoform expression or mitochondrial localization. No other changes in glycolytic enzymes were observed. LPS-mediated HK activation was not sufficient to increase glycolytic flux as indicated by reduced or unchanged pyruvate and lactate levels in the renal cortex. LPS-induced HK activation was associated with increased glucose-6-phosphate dehydrogenase activity but not glycogen production. Mechanistically, LPS-induced HK activation was attenuated by pharmacological inhibitors of the EGF receptor (EGFR) and Akt, indicating that EGFR/phosphatidylinositol 3-kinase/Akt signaling is responsible. Our findings reveal LPS rapidly increases renal cortical HK activity in an EGFR- and Akt-dependent manner and that HK activation is linked to increased pentose phosphate pathway activity.

Indexed as

Acute Kidney InjuryAnimalsEnzyme ActivationErbB ReceptorsGefitinibGlucosephosphate DehydrogenaseGlycolysisHeterocyclic Compounds, 3-RingHexokinaseKidney CortexLipopolysaccharidesMaleMicePentose Phosphate PathwayPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktErbB ReceptorsGefitinibGlucosephosphate DehydrogenaseHeterocyclic Compounds, 3-RingHexokinaseHK1 protein, mouseLipopolysaccharidesMK 2206Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktQuinazolinesacute kidney injuryEGFRhexokinaselipopolysaccharidepentose phosphate pathway

Identifiers

PMID24990892
PMCPMC4137133
OpenAlexW2049574005

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.