Apoptosis plays an indispensable role in biological processes of development, tissue homeostasis, and response to injury. Excessive apoptosis is associated with neurodegenerative diseases and response to myocardial ischemia, whereas defective apoptosis is linked to cancer and possibly cystic fibrosis. Similar studies in adult rabbit cardiomyocytes indicate that activation of this pump also confers protection against ischemic injury. Acidification may be necessary for activation of the endonuclease responsible for DNA degradation during apoptosis.
Mitochondrial function is greatly impaired during apoptosis.
In particular, cytochrome c is unable to participate in electron transport and may be co-opted to perform a new function, that of activation of death proteases. The basis for this change appears to be central to understanding the process of apoptosis. R.A. G-CSF upregulates the vacuolar proton ATPase in human neutrophils. B.M. Lack of release of cytochrome c from mitochondir into cytosol early in the course of Fas-mediated apoptosis of Jurkat cells.