apoptóze

Apoptosis, also known as programmed cell death, is a type of cell death that is a normal and controlled process in multicellular organisms. It plays a crucial role in various physiological and pathological processes, including development, tissue homeostasis, and immune response. Apoptosis is characterized by distinct morphological changes, such as cell shrinkage, nuclear fragmentation, and the formation of apoptotic bodies. These changes are accompanied by specific biochemical events, including the activation of caspases, a family of cysteine-aspartic acid proteases, and the cleavage of various cellular proteins.

Apoptosis can be induced by a variety of stimuli, including growth factor withdrawal, DNA damage, and exposure to certain toxins. The process is tightly regulated by a complex network of proteins, including members of the Bcl-2 family, which can either promote or inhibit apoptosis. The intrinsic pathway of apoptosis is initiated by the release of cytochrome c from the mitochondria, while the extrinsic pathway is triggered by the activation of death receptors on the cell surface.

Apoptosis is distinct from necrosis, another form of cell death, which is often characterized by cell swelling, membrane rupture, and the release of cellular contents. Unlike necrosis, apoptosis does not typically induce an inflammatory response and is generally considered a more "clean" form of cell death. However, in certain pathological conditions, such as ischemia-reperfusion injury, apoptosis can contribute to tissue damage and inflammation.

Apoptosis has been implicated in a wide range of diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. In cancer, for example, apoptosis is often dysregulated, leading to the accumulation of abnormal cells and the development of tumors. Understanding the mechanisms of apoptosis and its regulation is therefore of great interest in the fields of biology, medicine, and pharmacology.