Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2003 May 9;304(3):551-9.

Mitochondria and ischemic reperfusion damage in the adult and in the developing brain.

Author information

1
Department of Physiology, Perinatal Center, Göteborg University, P.O. Box 432, SE 405 30 Göteborg, Sweden. klas.blomgren@fysiologi.gu.se

Abstract

The developing and the adult brain respond in similar ways to ischemia, but also display clear differences. For example, the relative contributions of necrosis and apoptosis to neuronal death may be different, such that apoptotic mechanisms would be more prevalent in the developing brain. During normal development, more than half of the neurons in some brain regions are removed through apoptosis, and effectors like caspase-3 are highly upregulated in the immature brain. Mitochondria are pivotal regulators of cell death through their role in energy production and calcium homeostasis, their capacity to release apoptogenic proteins and to produce reactive oxygen species. This review will summarize some of the current studies dealing with mitochondria-related mechanisms of ischemic brain damage, with special reference to developmental aspects.

PMID:
12729590
DOI:
10.1016/s0006-291x(03)00628-4
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center