Evidence map›Paper›PMID 25264175›Full record

ReviewJournal of molecular and cellular cardiology2015

Hexokinases and cardioprotection.

Guillaume Calmettes, Bernard Ribalet, Scott John, Paavo Korge, Peipei Ping, James N Weiss

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. VDAC2: an emerging pivotal and multifaceted regulator in tumor biology.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Hexokinase 2 in Cancer: A Prima Donna Playing Multiple Characters.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Metabolomic Analysis of Biosynthesis Mechanism of ε-Polylysine Produced byFrontiers in bioengineering and biotechnology · 2021
    Article
  19. Article
  20. Knockout of VDAC1 in H9c2 Cells Promotes Oxidative Stress-Induced Cell Apoptosis through Decreased Mitochondrial Hexokinase II Binding and Enhanced Glycolytic Stress.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020
    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

6 authors at 1 institution in 1 country.

Guillaume CalmettesUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Bernard RibaletUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Scott JohnUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Paavo KorgeUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Peipei PingUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
James N WeissUCLA Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. Electronic address: jweiss@mednet.ucla.edu.
University of California, Los Angeles · US

Funding

Mitochondrial pathways in NO induced cardioprotectionR01HL101228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CAI, HUA LINDA, PING, PEIPEI · 2010 to 2013
$2.6M
Hexokinases and CardioprotectionR01HL117385 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PING, PEIPEI, WEISS, JAMES N · 2013 to 2016
$1.9M
NHLBI NIH HHS HL101228NHLBI NIH HHS R01 HL101228NHLBI NIH HHS R01 HL117385
6 · The paper itself

Abstract

As mediators of the first enzymatic step in glucose metabolism, hexokinases (HKs) orchestrate a variety of catabolic and anabolic uses of glucose, regulate antioxidant power by generating NADPH for glutathione reduction, and modulate cell death processes by directly interacting with the voltage-dependent anion channel (VDAC), a regulatory component of the mitochondrial permeability transition pore (mPTP). Here we summarize the current state-of-knowledge about HKs and their role in protecting the heart from ischemia/reperfusion (I/R) injury, reviewing: 1) the properties of different HK isoforms and how their function is regulated by their subcellular localization; 2) how HKs modulate glucose metabolism and energy production during I/R; 3) the molecular mechanisms by which HKs influence mPTP opening and cellular injury during I/R; and 4) how different metabolic and HK profiles correlate with susceptibility to I/R injury and cardioprotective efficacy in cancer cells, neonatal hearts, and normal, hypertrophied and failing adult hearts, and how these difference may guide novel therapeutic strategies to limit I/R injury in the heart. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease".

Indexed as

AnimalsGlucoseHeart DiseasesHexokinaseHumansIsoenzymesMetabolomeMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryMyocardiumNeoplasmsGlucoseHexokinaseIsoenzymesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreCardioprotectionHexokinaseIschemia/reperfusionPostconditioningPreconditioning

Identifiers

PMID25264175
PMCPMC4268312
OpenAlexW1993660246

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.