Evidence map›Paper›PMID 25278904›Full record

ReviewFrontiers in physiology2014

Bcl-xL in neuroprotection and plasticity.

Elizabeth A Jonas, George A Porter, Kambiz N Alavian

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Bcl-xL as a Modulator of Senescence and Aging.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
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  11. Review
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  15. BDNF signaling: Harnessing stress to battle mood disorder.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Nerve Protective Effect of Asiaticoside against Ischemia-Hypoxia in Cultured Rat Cortex Neurons.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

3 authors at 3 institutions in 2 countries.

Elizabeth A JonasSection of Endocrinology, Department of Internal Medicine, Yale University New Haven, CT, USA ; Department of Neurobiology, Yale University New Haven, CT, USA.
George A PorterDepartments of Pediatrics (Cardiology), University of Rochester Medical Center Rochester, NY, USA ; Internal Medicine (Aab Cardiovascular Research Institute), University of Rochester Medical Center Rochester, NY, USA ; Department of Pharmacology and Physiology, University of Rochester Medical Center Rochester, NY, USA.
Kambiz N AlavianDivision of Brain Sciences, Department of Medicine, Imperial College London London, UK.
Imperial College London · GBUniversity of Rochester Medical Center · USYale University · US

Funding

Mitochondrial Ion Channels in Hypoxic NeuronsR37NS045876 · NINDS · YALE UNIVERSITY · PI Elizabeth Ann Jonas · 2014 to 2026
$4.9M
Role of Bcl-xL in neuronal mitochondrial calcium dynamicsR21NS081786 · NINDS · YALE UNIVERSITY · PI ALAVIAN, KAMBIZ NASSIRPOUR, JONAS, ELIZABETH ANN · 2013 to 2014
$456k
NINDS NIH HHS R21 NS081786NINDS NIH HHS R37 NS045876
6 · The paper itself

Abstract

Accepted features of neurodegenerative disease include mitochondrial and protein folding dysfunction and activation of pro-death factors. Neurons that experience high metabolic demand or those found in organisms with genetic mutations in proteins that control cell stress may be more susceptible to aging and neurodegenerative disease. In neurons, events that normally promote growth, synapse formation, and plasticity are also often deployed to control neurotoxicity. Such protective strategies are coordinated by master stress-fighting proteins. One such specialized protein is the anti-cell death Bcl-2 family member Bcl-xL, whose myriad death-protecting functions include enhancement of bioenergetic efficiency, prevention of mitochondrial permeability transition channel activity, protection from mitochondrial outer membrane permeabilization (MOMP) to pro-apoptotic factors, and improvement in the rate of vesicular trafficking. Synapse formation and normal neuronal activity provide protection from neuronal death. Therefore, Bcl-xL brings about synapse formation as a neuroprotective strategy. In this review we will consider how this multi-functional master regulator protein uses many strategies to enhance synaptic and neuronal function and thus counteracts neurodegenerative stimuli.

Indexed as

apoptosiscalciummitochondriapermeability transition poresynaptic plasticity

Identifiers

PMID25278904
PMCPMC4166110
OpenAlexW2149362209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.