Cardiomyocytes and neurons are highly susceptible to ischemia-reperfusion injury; accordingly, considerable effort has been
devoted to elucidating the cellular mechanisms responsible for ischemia-reperfusion-induced cell death and developing novel strategies
to minimize ischemia-reperfusion injury. Maintenance of mitochondrial integrity is, without question, a critical determinant of cell fate.
However, there is emerging evidence of a novel and intriguing extension to this paradigm: mitochondrial dynamics (that is, changes in
mitochondrial morphology achieved by fission and fusion) may play an important but as-yet poorly understood role as a determinant of
cell viability. Focusing on heart and brain, our aims in this review are to provide a synopsis of the molecular mechanisms of fission and
fusion, summarize our current understanding of the complex relationships between mitochondrial dynamics and the pathogenesis of
ischemia-reperfusion injury, and speculate on the possibility that targeted manipulation of mitochondrial dynamics may be exploited for
the design of novel therapeutic strategies for cardio- and neuroprotection.
Keywords: Heart, brain, ischemia, infarction, reperfusion injury, mitochondrial fission, mitochondrial fusion, apoptosis.
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