Cerebral ischemia, caused by disturbance of the bloo supply to the brain, is a major cause of death in our days. Diabetes mellitus exacerbates neuronal death induced by an ischemic insult. It is important to characterize the underlying mechanism of the cell damage in order to design therapeutic agents. The purpose of this study is to summarize some of the intracellular events leading to aggravated cell injury after diabetic ischemia including mitochondrial dysfunction. Release of mitochondrial cytochrome c activates the cell death executioner caspase-3 protease resulting in the cleavage of poly-ADP ribose polymerase (PARP) involved in DNA repair. Mitochondrial dysfunction is associated with enhanced production of free radicals such as superoxide anion, nitric oxide and peroxynitrite after diabetic ischemic injury. Mitochondrial dysfunction affects not only neurons but also astrocytes, which play an important role in neuronal functions. Damage of these cells participates in the exaggerated brain damage after cerebral ischemia. In summary, diabetes mellitus enhances intracellular pathways activated by cerebral ischemia and leads to exaggerated brain damage in diabetic subjects.
|Translated title of the contribution||Influence of diabetes mellitus on cerebral ischemia and reperfusion injury|
|Number of pages||5|
|Publication status||Published - Oct 1 2006|
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