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2015 ; 6
(ä): 115
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Novel Cellular Mechanisms for Neuroprotection in Ischemic Preconditioning: A View
from Inside Organelles
#MMPMID26074868
Sisalli MJ
; Annunziato L
; Scorziello A
Front Neurol
2015[]; 6
(ä): 115
PMID26074868
show ga
Ischemic preconditioning represents an important adaptation mechanism of CNS,
which results in its increased tolerance to the lethal cerebral ischemia. The
molecular mechanisms responsible for the induction and maintenance of ischemic
tolerance in the brain are complex and not yet completely clarified. In the last
10?years, great attention has been devoted to unravel the intracellular pathways
activated by preconditioning and responsible for the establishing of the tolerant
phenotype. Indeed, recent papers have been published supporting the hypothesis
that mitochondria might act as master regulators of preconditioning-triggered
endogenous neuroprotection due to their ability to control cytosolic calcium
homeostasis. More interestingly, the demonstration that functional alterations in
the ability of mitochondria and endoplasmic reticulum (ER) managing calcium
homeostasis during ischemia, opened a new line of research focused to the role
played by mitochondria and ER cross-talk in the pathogenesis of cerebral ischemia
in order to identify new molecular mechanisms involved in the ischemic tolerance.
In line with these findings and considering that the expression of the three
isoforms of the sodium calcium exchanger (NCX), NCX1, NCX2, and NCX3, mainly
responsible for the regulation of Ca(2+) homeostasis, was reduced during cerebral
ischemia, it was investigated whether these proteins might play a role in
neuroprotection induced by ischemic tolerance. In this review, evidence
supporting the involvement of ER and mitochondria interaction within the
preconditioning paradigm will be provided. In particular, the key role played by
NCXs in the regulation of Ca(2+)-homeostasis at the different subcellular
compartments will be discussed as new molecular mechanism proposed for the
establishing of ischemic tolerant phenotype.
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