Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation
Uchino, Hiroyuki ; Kuroda, Yasuhiro ; Morota, Saori LU ; Hirabayashi, Go ; Ishii, Nagao ; Shibasaki, Futoshi ; Ikeda, Yukiho ; Hansson, Magnus J. and Elmer, Eskil LU
(2008)
In Journal of Anesthesia
22(3).
p.253-262
- Abstract
- Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function.... (More)
- Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function. However, no substantial breakthrough has been achieved in the quest to develop effective pharmacological neuroprotective therapy directed at tissues of the CNS. The current situation is unacceptable, and preservation of function and protection of the brain from terminal impairment will be a vital medical issue in the twenty-first century. To achieve this goal, it is critical to clarify the key mechanisms leading to neuronal cell death. Here, we discuss the importance of the calcineurin/immunophilin signal transduction pathway and mitochondrial involvement in the detrimental chain of events leading to neuronal degeneration. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1284917
- author
- Uchino, Hiroyuki
; Kuroda, Yasuhiro
; Morota, Saori
LU
; Hirabayashi, Go
; Ishii, Nagao
; Shibasaki, Futoshi
; Ikeda, Yukiho
; Hansson, Magnus J.
and Elmer, Eskil
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain, Cyclophilin, Calcineurin, Permeability transition, Mitochondria, Neuroprotection
- in
- Journal of Anesthesia
- volume
- 22
- issue
- 3
- pages
- 253 - 262
- publisher
- Springer
- external identifiers
-
- wos:000260112500009
- scopus:49749090449
- pmid:18685932
- ISSN
- 0913-8668
- DOI
- 10.1007/s00540-008-0617-3
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Laboratory for Experimental Brain Research (013041000)
- id
- 384e3c11-965d-4dcb-9820-0bb44d45a060 (old id 1284917)
- date added to LUP
- 2016-04-01 13:38:27
- date last changed
- 2022-01-27 20:15:11
@article{384e3c11-965d-4dcb-9820-0bb44d45a060,
abstract = {{Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function. However, no substantial breakthrough has been achieved in the quest to develop effective pharmacological neuroprotective therapy directed at tissues of the CNS. The current situation is unacceptable, and preservation of function and protection of the brain from terminal impairment will be a vital medical issue in the twenty-first century. To achieve this goal, it is critical to clarify the key mechanisms leading to neuronal cell death. Here, we discuss the importance of the calcineurin/immunophilin signal transduction pathway and mitochondrial involvement in the detrimental chain of events leading to neuronal degeneration.}},
author = {{Uchino, Hiroyuki and Kuroda, Yasuhiro and Morota, Saori and Hirabayashi, Go and Ishii, Nagao and Shibasaki, Futoshi and Ikeda, Yukiho and Hansson, Magnus J. and Elmer, Eskil}},
issn = {{0913-8668}},
keywords = {{Brain; Cyclophilin; Calcineurin; Permeability transition; Mitochondria; Neuroprotection}},
language = {{eng}},
number = {{3}},
pages = {{253--262}},
publisher = {{Springer}},
series = {{Journal of Anesthesia}},
title = {{Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation}},
url = {{http://dx.doi.org/10.1007/s00540-008-0617-3}},
doi = {{10.1007/s00540-008-0617-3}},
volume = {{22}},
year = {{2008}},
}