How might blocking apoptosis reduce damage after a loss of blood flow to the heart or brain?
Apoptosis is a mechanism of programmed cell death that can be triggered by mild cellular injury, such as ischemiaβa reduction in blood flow to tissues like the heart or brain.1
When blood flow is restricted, cells may experience stress that activates the cell's internal "death decision" pathways, often mediated by the BCL-2 protein family on the mitochondria. By inhibiting this process, researchers aim to prevent the unnecessary death of cells that might otherwise survive the period of restricted blood flow. Blocking apoptosis essentially stops the activation of caspase proteolytic enzymes, which are responsible for dismantling the cell's cytoskeleton and degrading DNA.1
Consequently, therapeutic intervention to inhibit apoptosis has the potential to dramatically limit tissue damage following ischemic events by preserving the viability of cells that would have been prematurely signaled to self-destruct.1