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Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration.
Mol Neurobiol. 2008 Aug; 38(1):78-100.MN

Abstract

Calpain is a ubiquitous calcium-sensitive protease that is essential for normal physiologic neuronal function. However, alterations in calcium homeostasis lead to persistent, pathologic activation of calpain in a number of neurodegenerative diseases. Pathologic activation of calpain results in the cleavage of a number of neuronal substrates that negatively affect neuronal structure and function, leading to inhibition of essential neuronal survival mechanisms. In this review, we examine the mechanistic underpinnings of calcium dysregulation resulting in calpain activation in the acute neurodegenerative diseases such as cerebral ischemia and in the chronic neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, prion-related encephalopathy, and amylotrophic lateral sclerosis. The premise of this paper is that analysis of the signaling and transcriptional consequences of calpain-mediated cleavage of its various substrates for any neurodegenerative disease can be extrapolated to all of the neurodegenerative diseases vulnerable to calcium dysregulation.

Authors+Show Affiliations

Department of Neurology, University of Pittsburgh School of Medicine, S-507, Biomedical Science Tower, Pittsburgh, PA 15213, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

18686046

Citation

Vosler, P S., et al. "Calpain-mediated Signaling Mechanisms in Neuronal Injury and Neurodegeneration." Molecular Neurobiology, vol. 38, no. 1, 2008, pp. 78-100.
Vosler PS, Brennan CS, Chen J. Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration. Mol Neurobiol. 2008;38(1):78-100.
Vosler, P. S., Brennan, C. S., & Chen, J. (2008). Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration. Molecular Neurobiology, 38(1), 78-100. https://doi.org/10.1007/s12035-008-8036-x
Vosler PS, Brennan CS, Chen J. Calpain-mediated Signaling Mechanisms in Neuronal Injury and Neurodegeneration. Mol Neurobiol. 2008;38(1):78-100. PubMed PMID: 18686046.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration. AU - Vosler,P S, AU - Brennan,C S, AU - Chen,J, Y1 - 2008/08/07/ PY - 2008/05/23/received PY - 2008/07/17/accepted PY - 2008/8/8/pubmed PY - 2008/10/16/medline PY - 2008/8/8/entrez SP - 78 EP - 100 JF - Molecular neurobiology JO - Mol Neurobiol VL - 38 IS - 1 N2 - Calpain is a ubiquitous calcium-sensitive protease that is essential for normal physiologic neuronal function. However, alterations in calcium homeostasis lead to persistent, pathologic activation of calpain in a number of neurodegenerative diseases. Pathologic activation of calpain results in the cleavage of a number of neuronal substrates that negatively affect neuronal structure and function, leading to inhibition of essential neuronal survival mechanisms. In this review, we examine the mechanistic underpinnings of calcium dysregulation resulting in calpain activation in the acute neurodegenerative diseases such as cerebral ischemia and in the chronic neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, multiple sclerosis, prion-related encephalopathy, and amylotrophic lateral sclerosis. The premise of this paper is that analysis of the signaling and transcriptional consequences of calpain-mediated cleavage of its various substrates for any neurodegenerative disease can be extrapolated to all of the neurodegenerative diseases vulnerable to calcium dysregulation. SN - 0893-7648 UR - https://www.unboundmedicine.com/medline/citation/18686046/Calpain_mediated_signaling_mechanisms_in_neuronal_injury_and_neurodegeneration_ L2 - https://dx.doi.org/10.1007/s12035-008-8036-x DB - PRIME DP - Unbound Medicine ER -