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Cited by 383

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death?

Sullivan, P.G., Rabchevsky, A.G., Waldmeier, P.C., Springer, J.E.·2005·Journal of Neuroscience Research
DOI 10.1002/jnr.20292
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Abstract

Experimental traumatic brain injury (TBI) and spinal cord injury (SCI) result in a rapid and significant necrosis of neuronal tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the primary damage, resulting in significant neurologic dysfunction. It is believed that alterations in excitatory amino acids (EAA), increased reactive oxygen species (ROS), and the disruption of Ca 2+ homeostasis are major factors contributing to the ensuing neuropathology. Mitochondria serve as the powerhouse of the cell by maintaining ratios of ATP:ADP that thermodynamically favor the hydrolysis of ATP to ADP + P i, yet a byproduct of this process is the generation of ROS. Proton‐pumping by components of the electron transport system (ETS) generates a membrane potential (ΔΨ) that can then be used to phosphorylate ADP or sequester Ca 2+ out of the cytosol into the mitochondrial matrix. This allows mitochondria to act as cellular Ca 2+ sinks and to be in phase with changes in cytosolic Ca 2+ levels. Under extreme loads of Ca 2+, however, opening of the mitochondrial permeability transition pore (mPTP) results in the extrusion of mitochondrial Ca 2+ and other high‐ and low‐molecular weight components. This catastrophic event discharges ΔΨ and uncouples the ETS from ATP production. Cyclosporin A (CsA), a potent immunosuppressive drug, inhibits mitochondrial permeability transition (mPT) by binding to matrix cyclophilin D and blocking its binding to the adenine nucleotide translocator. Peripherally administered CsA attenuates mitochondrial dysfunction and neuronal damage in an experimental rodent model of TBI, in a dose‐dependent manner. The underlying mechanism of neuroprotection afforded by CsA is most likely via interaction with the mPTP because the immunosuppressant FK506, which has no effect on the mPT, was not neuroprotective. When CsA was administrated after experimental SCI at the same dosage and regimen used TBI paradigms, however, it had no beneficial neuroprotective effects. This review takes a comprehensive and critical look at the evidence supporting the role for mPT in central nervous system (CNS) trauma and highlights the differential responses of CNS mitochondria to mPT induction and the implications this has for therapeutically targeting the mPT in TBI and SCI. © 2004 Wiley‐Liss, Inc.

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Metadata

Authors
Sullivan, P. G., Rabchevsky, A. G., Waldmeier, P. C., & Springer, J. E.
Venue
Journal of Neuroscience Research
Publisher
Wiley
Published
2004-11-30
Volume
79
Issue
1-2
Pages
231-239
ISSN
  • 0360-4012 (ISSN-L)
  • 1097-4547
DOI
10.1002/jnr.20292
OpenAlex
W2008225353
Cited by
383
References
9
FWCI
5.69
Type
journal article
Language
en
Open access
closed

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