Evidence map›Paper›PMID 24862206›Full record

ReviewJournal of vascular research2014

Mitochondrial mechanisms in cerebral vascular control: shared signaling pathways with preconditioning.

David W Busija, Prasad V Katakam

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of vascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Oxidative Stress and the Neurovascular Unit.Life (Basel, Switzerland) · 2021
    Review
  9. Precapillary sphincters and pericytes at first-order capillaries as key regulators for brain capillary perfusion.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Sexual differences in mitochondrial and related proteins in rat cerebral microvessels: A proteomic approach.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  11. Article
  12. Article
  13. SUR1-TRPM4 channels, not KNeuroscience letters · 2020
    Review
  14. Cerebrovascular function and mitochondrial bioenergetics after ischemia-reperfusion in male rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  15. Fetal Cerebral Artery Mitochondrion as Target of Prenatal Alcohol Exposure.International journal of environmental research and public health · 2019
    Review
  16. Article
  17. Review
  18. Article
  19. Insulin resistance in ischemic stroke.Metabolic brain disease · 2017
    Review
  20. Review
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

2 authors at 1 institution in 1 country.

David W BusijaDepartment of Pharmacology, Tulane University School of Medicine, New Orleans, La., USA.
Prasad V Katakam
Tulane University · US

Funding

Mitochondrial Influences on Cerebral ArteriesR01HL093554 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BUSIJA, DAVID W · 2009 to 2018
$3.3M
Potassium Channel Dysfunction in Cerebral ArteriesR01HL077731 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BUSIJA, DAVID W · 2004 to 2013
$3.2M
REGULATION OF CEREBRAL BLOOD FLOWR01HL030260 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BUSIJA, DAVID W · 1986 to 2010
$2.9M
Endothelial Dysfunction in Insulin ResistanceR01HL065380 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BUSIJA, DAVID W · 2002 to 2010
$2.5M
NHLBI NIH HHS HL-030260NHLBI NIH HHS HL-065380NHLBI NIH HHS HL-077731NHLBI NIH HHS HL-093554NHLBI NIH HHS R01 HL030260NHLBI NIH HHS R01 HL065380NHLBI NIH HHS R01 HL077731NHLBI NIH HHS R01 HL093554
6 · The paper itself

Abstract

Mitochondrial-initiated events protect the neurovascular unit against lethal stress via a process called preconditioning, which independently promotes changes in cerebrovascular tone through shared signaling pathways. Activation of adenosine triphosphate (ATP)-dependent potassium channels on the inner mitochondrial membrane (mitoKATP channels) is a specific and dependable way to induce protection of neurons, astroglia, and cerebral vascular endothelium. Through the opening of mitoKATP channels, mitochondrial depolarization leads to activation of protein kinases and transient increases in cytosolic calcium (Ca(2+)) levels that activate terminal mechanisms that protect the neurovascular unit against lethal stress. The release of reactive oxygen species from mitochondria has similar protective effects. Signaling elements of the preconditioning pathways also are involved in the regulation of vascular tone. Activation of mitoKATP channels in cerebral arteries causes vasodilation, with cell-specific contributions from the endothelium, vascular smooth muscles, and nerves. Preexisting chronic conditions, such as insulin resistance and/or diabetes, prevent preconditioning and impair relaxation to mitochondrial-centered responses in cerebral arteries. Surprisingly, mitochondrial activation after anoxic or ischemic stress appears to protect cerebral vascular endothelium and promotes the restoration of blood flow; therefore, mitochondria may represent an important, but underutilized target in attenuating vascular dysfunction and brain injury in stroke patients.

Indexed as

BenzimidazolesBrainBrain IschemiaCerebral ArteriesIschemic PreconditioningMembrane Potential, MitochondrialMitochondriaMuscle, Smooth, VascularPotassium ChannelsReactive Oxygen SpeciesSignal TransductionBenzimidazolesmitochondrial K(ATP) channelNS 1619Potassium ChannelsReactive Oxygen Species

Identifiers

PMID24862206
PMCPMC4149841
OpenAlexW2044201952

What OpenQuestion holds

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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.