[en] This review covers the general roles of members of the cysteine protease family of caspases in the process of apoptosis (programmed cell death) looking at their participation in both the "extrinsic" cell death receptor and the "intrinsic" mitochondrial cell death pathways. It defines the difference between initiator and effector caspases and shows the progression of caspase activations that ends up in the apoptotic cell death and elimination of a damaged cell. The review then presents what is currently know about the participation of caspases in the programmed cell death of inner ear sensory cells during the process of normal development and maturation of the inner ear and their importance in this process as illustrated by the results of caspase-3 gene knockout experiments. The participation of specific caspases and the sequence of their activation in the elimination (apoptosis) of damaged sensory cells from adult inner ears after an injury that generates oxidative stress are reviewed. Both the possibility and the potential efficacy of caspase inhibition with a broad-spectrum pancaspase inhibitor as an interventional therapy to treat and rescue oxidative stress-damaged inner ear sensory cells from apoptosis are presented and discussed.
Disciplines :
Otolaryngology Neurology
Author, co-author :
Van De Water, T. R.
Lallemend, François
Eshraghi, A. A.
Ahsan, S.
He, J.
Guzman, J.
Polak, M.
Malgrange, Brigitte ; Université de Liège - ULiège > CNCM/ Centre fac. de rech. en neurobiologie cell. et moléc.
Lefèbvre, Philippe ; Université de Liège - ULiège > Département des sciences cliniques > Oto-rhino-laryngologie et audiophonologie
Staecker, H.
Balkany, T. J.
Language :
English
Title :
Caspases, the enemy within, and their role in oxidative stress-induced apoptosis of inner ear sensory cells
Publication date :
July 2004
Journal title :
Otology and Neurotology
ISSN :
1531-7129
eISSN :
1537-4505
Publisher :
Lippincott Williams & Wilkins, Philadelphia, United States - Pennsylvania
Volume :
25
Issue :
4
Pages :
627-632
Peer reviewed :
Peer Reviewed verified by ORBi
Funders :
F.R.S.-FNRS - Fonds de la Recherche Scientifique [BE]
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