Evidence map›Paper›PMID 15377870›Full record

ReviewJournal of bioenergetics and biomembranes2004

Protection against ischemic brain injury by inhibition of mitochondrial oxidative stress.

Gary Fiskum, Robert E Rosenthal, Viktoria Vereczki, Erica Martin, Gloria E Hoffman, Christos Chinopoulos, Alicia Kowaltowski

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

65 citing papers in PubMed, 154 citations in OpenAlex.

  1. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Role of Excitatory Amino Acid Carrier 1 (International journal of molecular sciences · 2020
    Review
  11. Leonurine: From Gynecologic Medicine to Pleiotropic Agent.Chinese journal of integrative medicine · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mitochondrial dynamics following global cerebral ischemia.Molecular and cellular neurosciences · 2016
    Article

5 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

7 authors at 2 institutions in 2 countries.

Gary FiskumDepartment of Anesthesiology, University of Maryland School of Medicine, 685 W. Baltimore St., MSTF 5.34, Baltimore, Maryland 21201, USA. gfisk001@umaryland.edu
Robert E Rosenthal
Viktoria Vereczki
Erica Martin
Gloria E Hoffman
Christos Chinopoulos
Alicia Kowaltowski
University of Maryland, Baltimore · USUniversidade de São Paulo · BR

Funding

SPECTRIN-DEPENDENT MEMBRANE DOMAINS IN THE DEVELOPING CNSP01HD016596 · NICHD · UNIVERSITY OF MARYLAND BALTIMORE · PI MCKENNA, MARY C · 1985 to 2013
$12.8M
Molecular Mechanisms of Ischemia Reperfusion Brain InjuryR01NS034152 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FISKUM, GARY M · 1995 to 2008
$2.7M
Novel delivery of Bcl-2 for neuroprotectionR21NS045038 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FISKUM, GARY · 2003 to 2004
$353k
NICHD NIH HHS P01 HD016596NINDS NIH HHS R01 NS34152NINDS NIH HHS R21 NS45038
6 · The paper itself

Abstract

Mitochondria are both targets and sources of oxidative stress. This dual relationship is particularly evident in experimental paradigms modeling ischemic brain injury. One mitochondrial metabolic enzyme that is particularly sensitive to oxidative inactivation is pyruvate dehydrogenase. This reaction is extremely important in the adult CNS that relies very heavily on carbohydrate metabolism, as it represents the sole bridge between anaerobic and aerobic metabolism. Oxidative injury to this enzyme and to other metabolic enzymes proximal to the electron transport chain may be responsible for the oxidized shift in cellular redox state that is observed during approximately the first hour of cerebral reperfusion. In addition to impairing cerebral energy metabolism, oxidative stress is a potent activator of apoptosis. The mechanisms responsible for this activation are poorly understood but likely involve the expression of p53 and possibly direct effects of reactive oxygen species on mitochondrial membrane proteins and lipids. Mitochondria also normally generate reactive oxygen species and contribute significantly to the elevated net production of these destructive agents during reperfusion. Approaches to inhibiting pathologic mitochondrial generation of reactive oxygen species include mild uncoupling, pharmacologic inhibition of the membrane permeability transition, and simply lowering the concentration of inspired oxygen. Antideath mitochondrial proteins of the Bcl-2 family also confer cellular resistance to oxidative stress, paradoxically through stimulation of mitochondrial free radical generation and secondary upregulation of antioxidant gene expression.

Indexed as

Adaptation, PhysiologicalAnimalsApoptosisBrainBrain IschemiaCalciumCell HypoxiaCell RespirationHumansMitochondriaMitochondrial ProteinsModels, BiologicalNeuronsNeuroprotective AgentsOxidative StressPyruvate Dehydrogenase ComplexCalciumMitochondrial ProteinsNeuroprotective AgentsPyruvate Dehydrogenase ComplexReactive Oxygen Species

Identifiers

PMID15377870
OpenAlexW2028958046

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.