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Programmed cell death is important for normal physiological functioning, it is crucial in wound healing, development, differentiation and immune responses. However, unregulated cell death can lead to development of several diseases. Several forms of cell death include apoptosis, necrosis, and autophagy, which differ mainly in the cells morphological changes that accompany them, as well as the proteins involved in their activation and execution.

Apoptosis is the best characterized cell death process and it is often accompanied by plasma membrane blebbing, shrinkage or decrease in cell volume, chromatin condensation, and nuclear fragmentation. It usually involves activation of caspases, and is commonly divided into intrinsic or extrinsic pathways, depending on whether it is activated by the mitochondria with subsequent release of cytochrome C (intrinsic apoptotic pathway) or whether it is activated by death receptors (extrinsic apoptotic pathway). Besides the caspases, p53 is also known to be a major regulator of apoptosis.

Autophagy occurs with no chromatin condensation but involves vacuolization of the cytoplasm. It involves the retention of cytoplasmic material into autophagosomes for degradation by lysosomes. During autophagy, the autophagosomes fuse with the lysosomes to form autolysosomes, where the cytoplasmic content is then degraded by acidic hydrolases.

Necrosis, in contrast to apoptosis, is characterized by an increase in cell volume, and does not involve the activation of caspases. It involves swelling of organelles, rupture of the plasma membrane and leakage of intracellular components outside the cell. Necroptosis has been referred to as the programmed form of necrosis. All these forms of cell death can be activated independently of apoptosis, or if apoptosis fails. Other less known forms of cell death include pyroptosis, entosis, paraptosis, as well as others.

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