Evidence map›Paper›PMID 20129495›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2010

Calpain as a therapeutic target in traumatic brain injury.

Kathryn E Saatman, Jennifer Creed, Ramesh Raghupathi

Abstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

135 citing papers in PubMed, 220 citations in OpenAlex.

  1. Dual vulnerability of TDP-43 to calpain and caspase-3 proteolysis after neurotoxic conditions and traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014
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  14. Neuroprotective actions of norepinephrine in neurological diseases.Pflugers Archiv : European journal of physiology · 2024
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75 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

3 authors at 2 institutions in 1 country.

Kathryn E SaatmanSpinal Cord and Brain Injury Research Center, Department of Physiology, University of Kentucky, Lexington, Kentucky 40536-0509, USA. k.saatman@uky.edu
Jennifer Creed
Ramesh Raghupathi
Drexel University · USUniversity of Kentucky · US

Funding

Force Transmission in the Central Nervous SystemR01HD041699 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI MEANEY, DAVID F · 2001 to 2011
$6.3M
Role of calpastatin in modulating function following TBIP01NS058484 · NINDS · UNIVERSITY OF KENTUCKY · PI HALL, EDWARD D. · 2007 to 2011
$4.8M
Pathology-directed combination therapy for pediatric TBIR01HD061963 · NICHD · DREXEL UNIVERSITY · PI RAGHUPATHI, RAMESH · 2009 to 2013
$1.4M
NICHD NIH HHS HD41699NICHD NIH HHS R01 HD041699NICHD NIH HHS R01 HD061963NINDS NIH HHS NS058484NINDS NIH HHS P01 NS058484
6 · The paper itself

Abstract

The family of calcium-activated neutral proteases, calpains, appears to play a key role in neuropathologic events following traumatic brain injury (TBI). Neuronal calpain activation has been observed within minutes to hours after either contusive or diffuse brain trauma in animals, suggesting that calpains are an early mediator of neuronal damage. Whereas transient calpain activation triggers numerous cell signaling and remodeling events involved in normal physiological processes, the sustained calpain activation produced by trauma is associated with neuron death and axonal degeneration in multiple models of TBI. Nonetheless, the causal relationship between calpain activation and neuronal death is not fully understood. Much remains to be learned regarding the endogenous regulatory mechanisms for controlling calpain activity, the roles of different calpain isoforms, and the in vivo substrates affected by calpain. Detection of stable proteolytic fragments of the submembrane cytoskeletal protein alphaII-spectrin specific for cleavage by calpains has been the most widely used marker of calpain activation in models of TBI. More recently, these protein fragments have been detected in the cerebrospinal fluid after TBI, driving interest in their potential utility as TBI-associated biomarkers. Post-traumatic inhibition of calpains, either direct or indirect through targets related to intracellular calcium regulation, is associated with attenuation of functional and behavioral deficits, axonal pathology, and cell death in animal models of TBI. This review focuses on the current state of knowledge of the role of calpains in TBI-induced neuropathology and effectiveness of calpain as a therapeutic target in the acute post-traumatic period.

Indexed as

AnimalsBiomarkersBrain InjuriesCalpainHumansBiomarkersCalpain

Identifiers

PMID20129495
PMCPMC2842949
OpenAlexW2025275866

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.