Cell death

Cell death is the event of a biological cell ceasing to carry out its functions. This can occur through a natural, regulated process known as programmed cell death (PCD), which typically benefits the organism during its life-cycle. For instance, the separation of fingers and toes in a developing human embryo results from cells undergoing apoptosis, a form of PCD. Apoptosis, also called type I cell-death, involves characteristic morphological changes such as cell shrinkage, blebbing, nuclear fragmentation, chromatin condensation, and fragmentation of chromosomal DNA.

It is now understood that cells may be induced to actively commit suicide in a developmental context, while in a homeostatic context, the absence of certain survival factors can trigger the process. Another form of PCD is autophagy, or type II cell-death, which is cytoplasmic and marked by the formation of large vacuoles that degrade organelles in a specific sequence before the nucleus is destroyed. This catabolic process, often activated by nutrient deprivation, involves the autophagosomic-lysosomal breakdown of bulk cytoplasm, abnormal protein aggregates, and damaged organelles.

In contrast, necrosis is a non-physiological cell death resulting from infection or injury. The term "cell necrobiology" describes the life processes associated with the morphological, biochemical, and molecular changes that predispose, precede, and accompany cell death, as well as the subsequent tissue response. This term, derived from Greek roots meaning "death," "life," and "study," was initially coined to broadly define investigations of changes accompanying cell death, as detected by multiparameter flow- and laser scanning- cytometry.

Other non-apoptotic forms of programmed cell death exist, such as anoikis, cornification, excitotoxicity, ferroptosis, and Wallerian degeneration. Activation-induced cell death (AICD) is a PCD triggered by the interaction of Fas receptor and Fas ligand, helping maintain peripheral immune tolerance by negatively regulating activated T-lymphocytes. Ischemic cell death, or oncosis, is a passive, accidental form characterized by mitochondrial swelling and vacuolization.

Mitotic catastrophe is an oncosuppressive mechanism leading to cell death from premature or inappropriate entry into mitosis, common in cancer cells treated with ionizing radiation.