Evidence map›Paper›PMID 18039843›Full record

ArticleMolecular and cellular biology2008

Glucose phosphorylation and mitochondrial binding are required for the protective effects of hexokinases I and II.

Lin Sun, Shetha Shukair, Tejaswitha Jairaj Naik, Farzad Moazed, Hossein Ardehali

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

140 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Propionate Induces Energy Expenditure via Browning in Mesenteric Adipose Tissue.The Journal of clinical endocrinology and metabolism · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. ALPK2 prevents cardiac diastolic dysfunction in heart failure with preserved ejection fraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Metabolite signaling in the heart.Nature cardiovascular research · 2023
    Review

80 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Lin SunFeinberg Cardiovascular Institute, Northwestern University School of Medicine, Chicago, Illinois, USA.
Shetha Shukair
Tejaswitha Jairaj Naik
Farzad Moazed
Hossein Ardehali
Northwestern University · US

Funding

Role of the mitochondrial ATP-binding cassette protein-1 in cellular protectionR01HL087149 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 2007 to 2011
$2.1M
Functional Characterization of mABC1 ProteinK08HL079387 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI ARDEHALI, HOSSEIN · 2005 to 2009
$629k
NHLBI NIH HHS K08 HL079387NHLBI NIH HHS R01 HL087149
6 · The paper itself

Abstract

Alterations in glucose metabolism have been demonstrated for diverse disorders ranging from heart disease to cancer. The first step in glucose metabolism is carried out by the hexokinase (HK) family of enzymes. HKI and II can bind to mitochondria through their N-terminal hydrophobic regions, and their overexpression in tissue culture protects against cell death. In order to determine the relative contributions of mitochondrial binding and glucose-phosphorylating activities of HKs to their overall protective effects, we expressed full-length HKI and HKII, their truncated proteins lacking the mitochondrial binding domains, and catalytically inactive proteins in tissue culture. The overexpression of full-length proteins resulted in protection against cell death, decreased levels of reactive oxygen species, and possibly inhibited mitochondrial permeability transition in response to H(2)O(2). However, the truncated and mutant proteins exerted only partial effects. Similar results were obtained with primary neonatal rat cardiomyocytes. The HK proteins also resulted in an increase in the phosphorylation of voltage-dependent anion channel (VDAC) through a protein kinase Cepsilon (PKCepsilon)-dependent pathway. These results suggest that both glucose phosphorylation and mitochondrial binding contribute to the protective effects of HKI and HKII, possibly through VDAC phosphorylation by PKCepsilon.

Indexed as

AnimalsCell DeathCell LineGlucoseHexokinaseHumansMitochondriaMyocytes, CardiacPhosphorylationProtein Kinase C-epsilonRatsTransfectionVoltage-Dependent Anion ChannelsGlucoseHexokinaseHK1 protein, humanProtein Kinase C-epsilonVoltage-Dependent Anion Channels

Identifiers

PMID18039843
PMCPMC2223386
OpenAlexW2097990780

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.