%0 Journal Article %T Necrosis, a regulated mechanism of cell death La necrosis, un mecanismo regulado de muerte celular %A Mauricio Rojas L¨®pez %A Mar¨ªa Elena Ram¨ªrez Agudelo %J Iatreia %D 2010 %I Universidad de Antioquia %X Three types of cellular death have been defined by morphological and biochemical criteria: apoptosis, necrosis and autophagy. Apoptosis is a regulated cell death, mainly mediated by caspases; autophagy induces degradation of intracellular damaged organelles through the formation of vesicles that fuse with hydrolytic vacuoles. Necrosis has been traditionally defined by the rupture the cytoplasmic membrane with subsequent release of intracellular material, triggering localized inflammatory Intrinsic cellular activities and the events preceding cellular collapse are critical to determine the type of tissue damage. The fact that all three types of cellular death can coexist in any organ and tissue with different availabilities of ATP, suggests that necrosis can be conceived as an active event and that to some extent it may be regulated. Alterations in the structure of proteins and in the activity of different proteases, lipases and nucleases, indicate that each cell may have its own arsenal to trigger the events leading to necrosis. In this article we review some of the evidences on cellular regulation during necrosis. Con base en criterios morfol¨®gicos y bioqu¨ªmicos se han definido tres clases de muerte celular: apoptosis, autofagia y necrosis. La primera es una muerte celular regulada, mediada principalmente por caspasas; en la autofagia ocurre formaci¨®n de ves¨ªculas que se fusionan con vacuolas hidrol¨ªticas para degradar organelas intracelulares alteradas. En cuanto a la necrosis, se la ha definido tradicionalmente por la ruptura de la membrana citoplasm¨¢tica con salida del material intracelular lo que desencadena una reacci¨®n %K Apoptosis %K Autofagia %K Calcio %K Calpa¨ªnas %K Caspasas %K Fosfolipasas %K Mitocondria %K Necrosis %U http://www.iatreia.udea.edu.co/index.php/iatreia/article/view/1300