Abstract
Cell death represents the final outcome of several pathological conditions of the central nervous system and available evidence suggests that in both acute injuries and neurodegenerative diseases it is often associated with mitochondrial dysfunction. Thus, the possibility to prevent mitochondrial events involved in cell death might represent efficient tools to limit neuronal damage. In recent years, increased attention has been paid to the endogenous protein neuroglobin, since accumulating evidence showed that its high expression was associated with preserved mitochondrial function and to an increased survival of nerve cells in vitro and in vivo in a variety of experimental models of cell insult. The biological and structural features of neuroglobin and the mitochondria-related mechanisms of neuroglobin-induced neuroprotection will be here briefly discussed. In this respect, the inhibition of the intrinsic pathway of apoptosis emerges as a key neuroprotective effect induced by the protein. These findings could open the possibility to develop efficient neuroglobin-mediated therapeutic strategies aimed at minimizing the neuronal cell death occurring in impacting neurological pathologies like stroke and neurodegenerative diseases.
Highlights
Cell death represents the final outcome of several pathological conditions of the central nervous system (CNS), including acute neurological disorders and neurodegenerative diseases
Suggest that, irrespective of the type of its manifestation, cell death that occurs in the CNS in both acute injuries and neurodegenerative diseases is often associated with mitochondrial dysfunctions [4,5]
In the CNS, cell death is related with several diseases including cerebrovascular and traumatic events and neurodegenerative disorders
Summary
Cell death represents the final outcome of several pathological conditions of the central nervous system (CNS), including acute neurological disorders (such as cerebrovascular or traumatic events) and neurodegenerative diseases (such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and Huntington’s disease). The increased mitochondrial membrane permeability can trigger the mitochondrial-dependent (intrinsic) pathway of apoptosis (see [9] for a review) in which the released cytochrome c (Cyt-C) binds the apoptotic protease-activating factor 1 (APAF1), leading to the formation of a caspase activation platform (apoptosome). The apoptosome recruits and activates an initiator caspase (caspase-9), which, in turn, cleaves and activates the execution caspases (such as caspase-3 and caspase-7), leading to cytoskeletal reorganization and disintegration of the cell into apoptotic bodies Additional proteins, such as those from the Bcl family [10] and IAP (inhibitors of apoptosis proteins) family [11], can interfere with the pathway of apoptosis and the cell only commit to death if stress signals overcome all the protective measures. In the present review article, available evidence on NGB and on the possible mechanisms of action involved in NGB’s neuroprotection, with particular reference to its anti-apoptotic role, will be briefly summarized and discussed
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