See ((programmed cell death))
Regulation by growth factors and cytokines critical for health and helps avoid neoplastic disease.
It is a form of programmed cell death in multicellular organisms, and is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death.
Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types of programmed cell death (PCD) and involves a series of biochemical events leading to a characteristic cell morphology and death.
Cells die when excess and unwanted cells do not receive sufficient growth factor signals.
Ability of cells to survive in the absence of growth factors can lead to malignant transformation.
Serves many normal functions and is not necessarily associated with cell injury.
Principal feature is the shrinkage of the cell and its nucleus.
Necrosis of cells is associated with early loss of integrity of the plasma membrane, allowing influx of extra cellular clients and fluid while the cell and its organelles swell.
Plasma membrane integrity persists, played into the process of apoptosis,
Associated by cleavage of cytoskeleton proteins by specific proteases.
Features include collapse of sub cellular components, chromatin, nuclear fragmentation and formation of plasma membrane blebs.
Apoptosis, or Type I programmed cell death, is essential for the maintenance of normal cellular homeostasis and is an important physiological response to many forms of cellular stress.
Extrinsic apoptotic pathways occur when factors outside the cell activate cell surface death receptors (e.g., Fas) that result in the activation of caspases-8 or -10.
Intrinsic apoptotic pathways are a result from mitochondrial release of cytochrome c or endoplasmic reticulum malfunctions, each leading to the activation of caspase-9.
The nucleus and Golgi apparatus have damage sensors, which can lead the cells down apoptotic pathways.