Evidence map›Paper›PMID 23379852›Full record

ReviewExpert opinion on therapeutic targets2013

Targeting calpain in synaptic plasticity.

Michel Baudry, Maggie M Chou, Xiaoning Bi

Abstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-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

27 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Calpain-2 as a therapeutic target for acute neuronal injury.Expert opinion on therapeutic targets · 2018
    Review
  14. Article
  15. Calpain-GRIP Signaling in Nucleus Accumbens Core Mediates the Reconsolidation of Drug Reward Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Michel BaudryWestern University of Health Sciences, Graduate College of Biomedical Sciences, Basic Medical Sciences, COMP , 309 E 2nd St, Pomona, CA 91766, USA. mbaudry@westernu.edu
Maggie M Chou
Xiaoning Bi
Western University of Health Sciences · US

Funding

The Spine Cytoskeleton and Memory DisordersP01NS045260 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GALL, CHRISTINE M · 2003 to 2015
$14.4M
Simulation of learning: models and biological validationR01NS057128 · NINDS · WESTERN UNIVERSITY OF HEALTH SCIENCES · PI BAUDRY, MICHEL · 2009 to 2012
$2.2M
NINDS NIH HHS P01 NS045260NINDS NIH HHS P01NS045260-01NINDS NIH HHS R01 NS057128NINDS NIH HHS R01NS057128
6 · The paper itself

Abstract

introductionCalpains represent a family of neutral, calcium-dependent proteases, which modify the function of their target proteins by partial truncation. These proteases have been implicated in numerous cell functions, including cell division, proliferation, migration, and death. In the CNS, where µ-calpain and m-calpain are the main calpain isoforms, their activation has been linked to synaptic plasticity as well as to neurodegeneration. This review will focus on the role of calpains in synaptic plasticity and discuss the possibility of developing methods to manipulate calpain activity for therapeutic purposes. AREAS COVERED: This review covers the literature showing how calpains are implicated in synaptic plasticity and in a number of conditions associated with learning impairment. The possibility of developing new drugs targeting these enzymes for treating these conditions is discussed. EXPERT OPINION: As evidence accumulates that calpain activation participates in neurodegeneration and cancer, there is interest in developing therapeutic approaches using direct or indirect calpain inhibition. In particular, a peptide derived from the calpain truncation site of mGluR1α was shown to decrease neurodegeneration following neonatal hypoxia/ischemia. More selective approaches need to be developed to target calpain or some of its substrates for therapeutic indications associated with deregulation of synaptic plasticity.

Indexed as

AnimalsCalpainCytoskeletonHumansNeuronal PlasticityProtein BiosynthesisSynapsesCalpain

Identifiers

PMID23379852
PMCPMC4154356
OpenAlexW1998966218

What OpenQuestion holds

Textmetadata
LicenceTDM
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.