Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

In the cardiovascular system the two extreme modes of cell death apoptosis and necrosis as well as the intermediate forms such as autophagy are observed. It seems that the level of energy depletion determines the death program activated. Apoptosis is an important event occurring during cardiovascular disease initiation and progression. It is an energy-dependent, tightly regulated process in which cell death follows a programmed set of events. Early scientists of apoptotic cell death recognized its morphologic patterns which include nuclear pyknosis (highly condensed, well defined bodies within an intact nuclear envelope), cytoplasmic condensation, and cell shrinkage, followed by nuclear and cellular fragmentation and rapid phagocytosis of apoptotic bodies by adjacent cells in the absence of inflammation. Among other apoptotic processes DNA fragmentation is crucial to apoptotic cell death (Rich et al. 1999, Danial and Korsmeyer 2004). Programmed cell death is an essential process for tissue homeostasis; hence aberrant apoptotic activation is involved in the pathogenesis of atherosclerosis and heart failure. Multiple death and survival signals are integrated to generate molecular apoptotic pathways. The balance between pro-and anti-apoptotic signalling pathways determines the fate of a cell in response to the external or internal stimuli through the regulation of a kinase array. Apoptosis is integrated by three steps: cell membrane initiation step, intracellular pathway and execution step. The immediate objectives of apoptotic signalling are the activation of procaspases and the disabling of mitochondrial function. This is mediated by two pathways which are closely associated (Fig. 1).

Original publication





Book title

Apoptosis: Modern Insights into Disease from Molecules to Man

Publication Date



339 - 353