Programmed cell death, a controlled self-destruction used to remove damaged or unwanted cells.Apoptosis is a form of programmed cell death in which a cell dismantles itself in a controlled, orderly way. Unlike necrosis, where a cell swells and bursts and spills its contents into the surroundings, apoptosis keeps the cell's contents packaged so that neighbouring cells and immune cells can clear the debris without inflammation. The process is triggered by internal or external signals and follows a fixed sequence of steps, which is why it is described as programmed rather than accidental.
It matters because a multicellular organism constantly needs to remove cells it no longer wants: cells that are damaged, infected, or surplus. During development, apoptosis sculpts tissues — for example, it removes the webbing between the fingers of a human embryo. In adult tissues it balances cell division, so that organs keep a stable size. When apoptosis fails, damaged cells survive and can accumulate, which is one route toward cancer; when it runs too freely, tissues lose cells they need, as happens in some degenerative conditions.
Apoptosis explains how an organism can delete individual cells with precision, without harming its neighbours, and how cell number is kept in check. It also provides a clean way for the immune system to remove cells that are no longer useful, since the dying cell displays signals that mark it for uptake.
The term apoptosis was introduced in 1972 by John Kerr, Andrew Wyllie and Alastair Currie, who described a distinct form of cell death seen in tissues. The concept of programmed cell death during development had been observed earlier in insects, and the molecular machinery was worked out in the 1990s, including the role of caspases and the Bcl-2 family of regulators.
Two main routes lead to apoptosis. In the extrinsic route, an external death signal binds to a receptor on the cell surface, which activates a cascade of signalling proteins. In the intrinsic route, stress or damage inside the cell causes mitochondria to release certain proteins into the cytoplasm. Both routes converge on a family of enzymes called caspases, which are present in an inactive form and become active when cleaved. Once active, caspases cut structural and regulatory proteins, fragment the DNA, and break the cell into small membrane-bound packages. These packages expose molecules that attract phagocytic cells, which engulf them before any contents leak out.
Research on apoptosis underpins cancer therapy, since many treatments aim to push tumour cells into apoptosis, and it is used in studies of tissue development, immune tolerance and degenerative disease.
The word apoptosis comes from a Greek term for the falling of leaves from a tree, chosen to suggest a natural shedding of cells.