Evidence map›Paper›PMID 18685932›Full record

ReviewJournal of anesthesia2008

Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation.

Hiroyuki Uchino, Yasuhiro Kuroda, Saori Morota, Go Hirabayashi, Nagao Ishii, Futoshi Shibasaki, Yukiho Ikeda, Magnus J Hansson, Eskil Elmér

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of anesthesia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Blockade of acid-sensing ion channels protects articular chondrocytes from acid-induced apoptotic injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Article
  7. Article
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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

9 authors at 6 institutions in 2 countries.

Hiroyuki UchinoDepartment of Anesthesiology, Hachioji Medical Center, Tokyo Medical University, 1163 Tate-machi, Hachioji, Tokyo 193-0998, Japan.
Yasuhiro Kuroda
Saori Morota
Go Hirabayashi
Nagao Ishii
Futoshi Shibasaki
Yukiho Ikeda
Magnus J Hansson
Eskil Elmér
Lund University · SETokyo Medical University · JPTokyo Medical University Hachioji Medical Center · JPKagawa University Hospital · JPTokyo Metropolitan Institute of Medical Science · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function. However, no substantial breakthrough has been achieved in the quest to develop effective pharmacological neuroprotective therapy directed at tissues of the CNS. The current situation is unacceptable, and preservation of function and protection of the brain from terminal impairment will be a vital medical issue in the twenty-first century. To achieve this goal, it is critical to clarify the key mechanisms leading to neuronal cell death. Here, we discuss the importance of the calcineurin/immunophilin signal transduction pathway and mitochondrial involvement in the detrimental chain of events leading to neuronal degeneration.

Indexed as

Brain InjuriesCalcineurinCalcineurin InhibitorsCalciumCell DeathCyclophilinsHumansMitochondrial DiseasesMitochondrial MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreNerve DegenerationPeptidyl-Prolyl Isomerase FSignal TransductionVoltage-Dependent Anion ChannelsCalcineurinCalcineurin InhibitorsCalciumCyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FVoltage-Dependent Anion Channels

Identifiers

PMID18685932
OpenAlexW2014239093

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.