The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Viral Control of Mitochondrial Apoptosis
Open accessAbstract
Throughout the process of pathogen-host co-evolution, viruses have developed a battery of distinct strategies to overcome biochemical and immunological defenses of the host. Thus, viruses have acquired the capacity to subvert host cell apoptosis, control inflammatory responses, and evade immune reactions. Since the elimination of infected cells via programmed cell death is one of the most ancestral defense mechanisms against infection, disabling host cell apoptosis might represent an almost obligate step in the viral life cycle. Conversely, viruses may take advantage of stimulating apoptosis, either to kill uninfected cells from the immune system, or to induce the breakdown of infected cells, thereby favoring viral dissemination. Several viral polypeptides are homologs of host-derived apoptosis-regulatory proteins, such as members of the Bcl-2 family. Moreover, viral factors with no homology to host proteins specifically target key components of the apoptotic machinery. Here, we summarize the current knowledge on the viral modulation of mitochondrial apoptosis, by focusing in particular on the mechanisms by which viral proteins control the host cell death apparatus.
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Citations
Cites
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Self-citationShimizu, S., Narita, M., Tsujimoto, Y., & Tsujimoto, Y. (1999) · Nature · doi:10.1038/20959 · Cited by 2,178
Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis
Chipuk, J. E., Kuwana, T., Bouchier-Hayes, L., Droin, N. M., Newmeyer, D. D., Schuler, M., & Green, D. R. (2004) · Science · doi:10.1126/science.1092734 · Cited by 2,108 · cited 1×
“Impaired MMP is associated with multiple pathological conditions, including autoimmune diseases and cancer [S19]. Conversely, unscheduled MMP contributes to the development of diseases characterized by an excess of cell death, such as ischemia/reperfusion injuries, trauma, toxic/metabolic syndromes as well as chronic…”
BackgroundChen, L., Willis, S. N., Wei, A., Smith, B. J., Fletcher, J. I., Hinds, M. G., Colman, P. M., Day, C. L., Adams, J. M., & Huang, D. C. S. (2005) · Molecular Cell · doi:10.1016/j.molcel.2004.12.030 · Cited by 1,816
Letai, A., Bassik, M. C., Walensky, L. D., Sorcinelli, M. D., Weiler, S., & Korsmeyer, S. J. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00127-7 · Cited by 1,677
Nakagawa, T., Shimizu, S., Watanabe, T., Yamaguchi, O., Otsu, K., Yamagata, H., Inohara, H., Kubo, T., & Tsujimoto, Y. (2005) · Nature · doi:10.1038/nature03317 · Cited by 1,635
p53- and Drug-Induced Apoptotic Responses Mediated by BH3-Only Proteins Puma and Noxa
Villunger, A., Michalak, E. M., Coultas, L., Müllauer, F., Böck, G., Ausserlechner, M. J., Adams, J. M., & Strasser, A. (2003) · Science · doi:10.1126/science.1090072 · Cited by 1,327
Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of Apoptosis
Marzo, I., Brenner, C., Zamzami, N., Jürgensmeier, J. M., Susin, S. A., Vieira, H. L. A., Prévost, M.-C., Xie, Z., Matsuyama, S., Reed, J. C., et al. (1998) · Science · doi:10.1126/science.281.5385.2027 · Cited by 1,168
Self-citationThe ADP/ATP translocator is not essential for the mitochondrial permeability transition pore
Kokoszka, J. E., Waymire, K. G., Levy, S. E., Sligh, J. E., Cai, J., Jones, D. P., MacGregor, G. R., & Wallace, D. C. (2004) · Nature · doi:10.1038/nature02229 · Cited by 1,086
Mitochondrial apoptosis without VDAC
Galluzzi, L., & Kroemer, G. (2007) · Nature Cell Biology · doi:10.1038/ncb0507-487 · Cited by 91
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Cited by
Immunogenic Cell Death in Cancer Therapy
Kroemer, G., Galluzzi, L., Kepp, O., & Zitvogel, L. (2013) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032712-100008 · Cited by 3,303
Self-citationImmunogenic cell death in cancer and infectious disease
Galluzzi, L., Buqué, A., Kepp, O., Zitvogel, L., & Kroemer, G. (2017) · Nature Reviews Immunology · doi:10.1038/nri.2016.107 · Cited by 3,119
Self-citationImmunogenic cell stress and death
Kroemer, G., Galassi, C., Zitvogel, L., & Galluzzi, L. (2022) · Nature Immunology · doi:10.1038/s41590-022-01132-2 · Cited by 1,353
Self-citationDecoding cell death signals in liver inflammation
Brenner, C., Galluzzi, L., Kepp, O., & Kroemer, G. (2013) · Journal of Hepatology · doi:10.1016/j.jhep.2013.03.033 · Cited by 1,022
Self-citationAutophagy-Independent Functions of the Autophagy Machinery
Galluzzi, L., & Green, D. R. (2019) · Cell · doi:10.1016/j.cell.2019.05.026 · Cited by 863
“Such strategies go beyond the simple inhibition of autophagic flux, which would suppress the autophagic disposal of cytosolic virions but at the same time would render host cells considerably more sensitive to undergo premature apoptotic cell death and potentially compromise viral replication (Galluzzi et al., 2008; L…”
BackgroundSelf-citation
Metadata
- Authors
- Galluzzi, L., Brenner, C., Morselli, E., Touat, Z., & Kroemer, G.
- Venue
- PLoS Pathogens
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-05-30
- Volume
- 4
- Issue
- 5
- Pages
- e1000018
- ISSN
- 1553-7366 (ISSN-L)
- 1553-7374
- OpenAlex
- W2032206556
- Cited by
- 427
- References
- 10
- FWCI
- 11.54
- Type
- journal article
- Language
- en
- Open access
- gold
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