Molecular Markers of Caspase-Dependent and Mitochondrial Apoptosis: Role in the Development of Pathology and Cellular Senescence

Abstract

The data on the molecular mechanisms of normal and pathological apoptosis are summarized. Three phases of apoptosis are distinguished: signal, effector, and degradation. The signal phase includes the extrinsic (caspase-dependent) and extrinsic (mitochondrial) pathways. Molecular markers of extrinsic and extrinsic apoptotic pathways play an important role in the diagnostics and treatment of immune, bronchopulmonary, excretory, and cardiovascular system pathologies, oncology, and senescence. This review considers the initiator caspases-8 and -9 and the effector caspase-3 as the molecular markers of the caspase-dependent apoptosis. The main molecular markers of the mitochondrial (or caspase-independent) apoptosis are p53, p21, and p16 proteins, which respond to DNA damage and are involved in cellular senescence, as well as chaperon prohibitin and flavoprotein apoptosis-inducing factor.