Cristae remodeling and mitochondrial fragmentation: A checkpoint for cytochrome c release and apoptosis?

Abstract

A crucial amplificatory event in several apoptotic cascades is the complete release of cytochrome c from mitochondria. This is accomplished by the activation of multidomain proapoptotic members of the Bcl-2 family and accompanied by changes in the internal structure of mitochondria, a process known as cristae remodelling, and by mitochondrial fragmentation. Here we illustrate the role of dynamin-related proteins controlling mitochondrial morphology in the regulation of cristae remodelling, organelle fragmentation, cytochrome c release, apoptosis and genetic diseases like dominant optic atrophy; and discuss the controversies on their functional role in apoptosis, with an outlook on the possible exploitation of the inhibition of these proteins in cancer chemotherapy.