Cell Cycle Proteins and Retinal Degeneration: Evidences of New Potential Therapeutic Targets.
Details
Serval ID
serval:BIB_28E6505575E0
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Cell Cycle Proteins and Retinal Degeneration: Evidences of New Potential Therapeutic Targets.
Journal
Advances In Experimental Medicine and Biology
ISSN
0065-2598 (Print)
ISSN-L
0065-2598
Publication state
Published
Issued date
2016
Peer-reviewed
Oui
Volume
854
Pages
371-377
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Abstract
During different forms of neurodegenerative diseases, including the retinal degeneration, several cell cycle proteins are expressed in the dying neurons from Drosophila to human revealing that these proteins are a hallmark of neuronal degeneration. This is true for animal models of Alzheimer's, and Parkinson's diseases, Amyotrophic Lateral Sclerosis and for Retinitis Pigmentosa as well as for acute injuries such as stroke and light damage. Longitudinal investigation and loss-of-function studies attest that cell cycle proteins participate to the process of cell death although with different impacts, depending on the disease. In the retina, inhibition of cell cycle protein action can result to massive protection. Nonetheless, the dissection of the molecular mechanisms of neuronal cell death is necessary to develop adapted therapeutic tools to efficiently protect photoreceptors as well as other neuron types.
Keywords
Animals, Apoptosis/drug effects, Cell Cycle Proteins/antagonists & inhibitors, Cell Cycle Proteins/metabolism, Cell Death/drug effects, Cell Division/drug effects, Drug Therapy/methods, Humans, Molecular Targeted Therapy/methods, Neurons/drug effects, Neurons/metabolism, Photoreceptor Cells/drug effects, Photoreceptor Cells/metabolism, Retinal Degeneration/drug therapy, Retinal Degeneration/metabolism
Pubmed
Web of science
Create date
05/10/2015 10:52
Last modification date
20/08/2019 13:08