Cyclophilin-D inhibition in neuroprotection : dawn of a new era of mitochondrial medicine
Uchino, Hiroyuki LU ; Hatakeyama, Kiyoshi ; Morota, Saori LU ; Tanoue, Tadashi ; Nishiyama, Takahisa ; Usui, Daiki ; Taguchi, Chisato ; Suzuki, Morika ; Hansson, Magnus J LU
and Elmér, Eskil
LU
(2013)
In Acta Neurochirurgica. Supplementum
118.
p.5-311
- Abstract
Traumatic brain injury and ischemia can result in marked neuronal degeneration and residual impairment of cerebral function. However, no effective pharmacological treatment directed at tissues of the central nervous system (CNS) for acute intervention has been developed. The detailed pathophysiological cascade leading to -neurodegeneration in these conditions has not been elucidated, but cellular calcium overload and mitochondrial dysfunction have been implicated in a wide range of animal models involving degeneration of the CNS. In particular, activation of the calcium-induced mitochondrial permeability transition (mPT) is considered to be a major cause of cell death inferred by the broad and potent neuroprotective effects of... (More)
Traumatic brain injury and ischemia can result in marked neuronal degeneration and residual impairment of cerebral function. However, no effective pharmacological treatment directed at tissues of the central nervous system (CNS) for acute intervention has been developed. The detailed pathophysiological cascade leading to -neurodegeneration in these conditions has not been elucidated, but cellular calcium overload and mitochondrial dysfunction have been implicated in a wide range of animal models involving degeneration of the CNS. In particular, activation of the calcium-induced mitochondrial permeability transition (mPT) is considered to be a major cause of cell death inferred by the broad and potent neuroprotective effects of -pharmacological inhibitors of mPT, especially modulators of cyclophilin activity and, more specifically, genetic inactivation of the mitochondrial cyclophilin, cyclophilin D. Reviewed are evidence and challenges that could bring on the dawning of mitochondrial medicine aimed at safeguarding energy supply following acute injury to the CNS.
(Less)
- author
- Uchino, Hiroyuki
LU
; Hatakeyama, Kiyoshi
; Morota, Saori
LU
; Tanoue, Tadashi
; Nishiyama, Takahisa
; Usui, Daiki
; Taguchi, Chisato
; Suzuki, Morika
; Hansson, Magnus J
LU
and Elmér, Eskil
LU
- organization
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Animals, Arsenicals, Brain Injuries, Calcium, Cyclophilins, Cyclosporine, Enzyme Inhibitors, Humans, Ischemia, Mitochondria, Neuroprotective Agents
- in
- Acta Neurochirurgica. Supplementum
- volume
- 118
- pages
- 5 pages
- publisher
- Springer
- external identifiers
-
- pmid:23564156
- scopus:84881341425
- ISSN
- 0065-1419
- DOI
- 10.1007/978-3-7091-1434-6_61
- language
- English
- LU publication?
- yes
- id
- 4b7e7e91-7b6e-4825-aecb-57290e95cc46
- date added to LUP
- 2016-08-29 12:32:28
- date last changed
- 2024-06-01 14:56:34
@article{4b7e7e91-7b6e-4825-aecb-57290e95cc46,
abstract = {{<p>Traumatic brain injury and ischemia can result in marked neuronal degeneration and residual impairment of cerebral function. However, no effective pharmacological treatment directed at tissues of the central nervous system (CNS) for acute intervention has been developed. The detailed pathophysiological cascade leading to -neurodegeneration in these conditions has not been elucidated, but cellular calcium overload and mitochondrial dysfunction have been implicated in a wide range of animal models involving degeneration of the CNS. In particular, activation of the calcium-induced mitochondrial permeability transition (mPT) is considered to be a major cause of cell death inferred by the broad and potent neuroprotective effects of -pharmacological inhibitors of mPT, especially modulators of cyclophilin activity and, more specifically, genetic inactivation of the mitochondrial cyclophilin, cyclophilin D. Reviewed are evidence and challenges that could bring on the dawning of mitochondrial medicine aimed at safeguarding energy supply following acute injury to the CNS.</p>}},
author = {{Uchino, Hiroyuki and Hatakeyama, Kiyoshi and Morota, Saori and Tanoue, Tadashi and Nishiyama, Takahisa and Usui, Daiki and Taguchi, Chisato and Suzuki, Morika and Hansson, Magnus J and Elmér, Eskil}},
issn = {{0065-1419}},
keywords = {{Animals; Arsenicals; Brain Injuries; Calcium; Cyclophilins; Cyclosporine; Enzyme Inhibitors; Humans; Ischemia; Mitochondria; Neuroprotective Agents}},
language = {{eng}},
pages = {{5--311}},
publisher = {{Springer}},
series = {{Acta Neurochirurgica. Supplementum}},
title = {{Cyclophilin-D inhibition in neuroprotection : dawn of a new era of mitochondrial medicine}},
url = {{http://dx.doi.org/10.1007/978-3-7091-1434-6_61}},
doi = {{10.1007/978-3-7091-1434-6_61}},
volume = {{118}},
year = {{2013}},
}