Putative roles of mitochondrial Voltage-Dependent Anion Channel, Bcl-2 family proteins and c-Jun N-terminal Kinases in ischemic stroke associated apoptosis.

There is a constant need for better stroke treatments. Neurons at the periphery of an ischemic stroke affected brain tissue remains metabolically active for several hours or days after stroke onset. They later undergo mitochondrion-mediated apoptosis. It has been found that inhibiting apoptosis in the peripheral ischemic neurons could be very effective in the prevention of stroke progression. During stroke associated apoptosis, cytosolic c-Jun N-terminal Kinases (JNKs) and Bcl-2 family proteins translocate towards mitochondria and promote cytochrome c release by interacting with the outer mitochondrion membrane associated proteins. This review provides an overview of the plausible interactions of the outer mitochondrial membrane Voltage Dependent Anion Channel, Bcl-2 family proteins and JNKs in cytochrome c release in the peripheral ischemic stroke associated apoptotic neurons. The review ends with a note on designing new anti-stroke treatments.