Open Access

REVIEW

Review: Mitochondrial apoptotic pathways

NORA MOHAMAD, ALICIA GUTIÉRREZ, MARIEL NÚÑEZ, CLAUDIA COCCA, GABRIELA MARTÍN*, GRACIELA CRICCO, VANINA MEDINA, ELENA RIVERA, ROSA BERGOC*.

Radioisotopes Laboratory, School of Pharmacy and Biochemistry, University of Buenos Aires. Buenos Aires, Argentina.
* Members of CONICET
Address correspondence to: Prof. Rosa M. Bergoc, PhD. Laboratorio de Radioisótopos, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires. Junín 956 (1113) Buenos Aires, ARGENTINA. FAX: (+54-11) 4964-8202 / 4743-2857. E-mail: rmbergoc@arnet.com.ar / rmbergoc@ffyb.uba.ar

BIOCELL 2005, 29(2), 149-161. https://doi.org/10.32604/biocell.2005.29.149

Abstract

Apoptosis or programmed cell death (PCD) is a physiological process characteristic of pluricellular organisms leading to self-destruction of the cell. It is therefore involved in development, homeostasis and host defense. However, a significant difference has been shown between mammalian cell apoptosis and non-mammalian cell apoptosis: mitochondria are implicated only in the former. Execution of PCD includes the release of several proapoptotic proteins from the intermembrane space of mitochondria. They could exert their actions through a caspase dependent as well as a caspase independent way. On the other hand, regulation of PCD is mainly given by the Bcl-2 family members, which are in turn essentially regulated by activation of death receptors and/or DNA damage. Nowadays, execution of apoptosis is better known than its regulation. Nevertheless, we are still far of a complete understanding of the apoptotic process.

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