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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.

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author
organization
publishing date
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
  • 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
2016-10-30 04:49:30
@misc{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},
  keyword      = {Animals,Arsenicals,Brain Injuries,Calcium,Cyclophilins,Cyclosporine,Enzyme Inhibitors,Humans,Ischemia,Mitochondria,Neuroprotective Agents},
  language     = {eng},
  pages        = {5--311},
  publisher    = {ARRAY(0x98ab080)},
  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},
  volume       = {118},
  year         = {2013},
}