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Apoptosis - Programmed Cell Death

Vilim Žlender


Puni tekst: hrvatski pdf 517 Kb

str. 267-274

preuzimanja: 16.908

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Sažetak

During the evolution, multi-cellular organisms have developed various protective mechanisms against environmental insults. Apoptosis is one of physiological mechanisms where in fact a cell itself actively induces its own death. In contrast to necrosis where the cell death occurs usually as a result of severe physical or chemical extra cellular factors accompanied by inflammatory reactions of tissue, the apoptotic process starts without signs and symptoms of inflammation, and generally starts from the inside of the cell, involving the use of energy and active synthesis of specific proteins. Apoptosis is important for the right balance between the loss of old, non-functional cells and the formation of new ones in certain organs and tissues. In adition, it is a specific answer of an organism to a number of pathological conditions. Thus apoptosis plays a very important role both in physiologic and pathologic processes in the body throughout the life of an organism. A normal development of embryo and foetus is impossible without a very intensive apoptotic process. The dysfunction of the apoptotic mechanism is associated with a number of diseases in humans and animals. The apoptosis starts by triggering different intra- and intercellular signals and stimulations, which involve a number of extrinsic or intrinsic apoptotic pathways resulting in caspase cascade activation. Caspases belongs to the family of cisteine proteases, and have a central role in facilitating a number of morphological and biochemical changes during the programmed cell death. The understanding of these complex pathways offers new approaches to clinical treatment of fatal human diseases. The promising possibilities of application of the knowledge about the mechanism of apoptosis in the treatment of human diseases make the research in this field challenging and exciting.

Ključne riječi

Bcl-2 family; caspases; homeostasis; death receptors; necrosis; p53

Hrčak ID:

344

URI

https://hrcak.srce.hr/344

Datum izdavanja:

4.2.2004.

Podaci na drugim jezicima: hrvatski

Posjeta: 25.389 *