Death by design: apoptosis, necrosis and autophagy.

Apoptosis is the principal mechanism by which cells are physiologically eliminated in metazoan organisms. During apoptotic death, cells are neatly carved up by caspases and packaged into apoptotic bodies as a mechanism to avoid immune activation. Recently, necrosis, once thought of as simply a passive, unorganized way to die, has emerged as an alternate form of programmed cell death whose activation might have important biological consequences, including the induction of an inflammatory response. Autophagy has also been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy in times of stress. Recent advances have helped to define the function of and mechanism for programmed necrosis and the role of autophagy in cell survival and suicide.

[1]  G. Kroemer,et al.  A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL-positive human leukemic cells: caspase-independent, necrosis-like programmed cell death mediated by serine protease activity. , 2004, Blood.

[2]  A. Kimchi,et al.  Autophagy as a cell death and tumor suppressor mechanism , 2004, Oncogene.

[3]  B. Moss,et al.  A Role for Tumor Necrosis Factor Receptor-2 and Receptor-interacting Protein in Programmed Necrosis and Antiviral Responses* , 2003, Journal of Biological Chemistry.

[4]  Jayanta Debnath,et al.  Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is required for induction of autophagy during lumen formation in vitro. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[5]  J. Tschopp,et al.  Caspase-independent cell death in T lymphocytes , 2003, Nature Immunology.

[6]  S. Snyder,et al.  Poly(ADP-ribose) polymerase is a mediator of necrotic cell death by ATP depletion. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[7]  E. Baehrecke Autophagic programmed cell death in Drosophila , 2003, Cell Death and Differentiation.

[8]  Ajjai Alva,et al.  Regulation of an ATG7-beclin 1 Program of Autophagic Cell Death by Caspase-8 , 2004, Science.

[9]  Marcel Leist,et al.  Cathepsin B Acts as a Dominant Execution Protease in Tumor Cell Apoptosis Induced by Tumor Necrosis Factor , 2001, The Journal of cell biology.

[10]  Brian Seed,et al.  Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule , 2000, Nature Immunology.

[11]  C. Thompson,et al.  Defective autophagy leads to cancer. , 2003, Cancer cell.

[12]  J. Golden,et al.  The Proapoptotic Activities of Bax and Bak Limit the Size of the Neural Stem Cell Pool , 2003, The Journal of Neuroscience.

[13]  V. Gabai,et al.  Necrosis: a specific form of programmed cell death? , 2003, Experimental cell research.

[14]  Daniel J Klionsky,et al.  Development by self-digestion: molecular mechanisms and biological functions of autophagy. , 2004, Developmental cell.

[15]  Alexei Degterev,et al.  Diversity in the Mechanisms of Neuronal Cell Death , 2003, Neuron.

[16]  C. Kitanaka,et al.  Caspase-independent programmed cell death with necrotic morphology. , 1999, Cell death and differentiation.

[17]  W. Zong,et al.  Alkylating DNA damage stimulates a regulated form of necrotic cell death. , 2004, Genes & development.

[18]  R. Lockshin,et al.  Caspase-independent cell death? , 2004, Oncogene.

[19]  Arnold J. Levine,et al.  Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[20]  Jayanta Debnath,et al.  The Role of Apoptosis in Creating and Maintaining Luminal Space within Normal and Oncogene-Expressing Mammary Acini , 2002, Cell.

[21]  H. Nakayama,et al.  A serine protease, HtrA2, is released from the mitochondria and interacts with XIAP, inducing cell death. , 2001, Molecular cell.

[22]  S. Emr,et al.  Autophagy as a regulated pathway of cellular degradation. , 2000, Science.

[23]  S. Korsmeyer,et al.  Review Cell Death: Critical Control Points Another Line of Evidence for the Importance of Caspases in Cell Death Came From , 2022 .

[24]  J P Schellens,et al.  The phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002 inhibit autophagy in isolated rat hepatocytes. , 1997, European journal of biochemistry.

[25]  W. Fiers,et al.  More than one way to die: apoptosis, necrosis and reactive oxygen damage , 1999, Oncogene.

[26]  Govind Bhagat,et al.  Promotion of tumorigenesis by heterozygous disruption of the beclin 1 autophagy gene. , 2003, The Journal of clinical investigation.

[27]  S. Korsmeyer,et al.  Placement of the BCL2 Family Member BAX in the Death Pathway of Sympathetic Neurons Activated by Trophic Factor Deprivation , 1998, Experimental Neurology.

[28]  W. Fiers,et al.  Inhibition of Caspases Increases the Sensitivity of L929 Cells to Necrosis Mediated by Tumor Necrosis Factor , 1998, The Journal of experimental medicine.