Cell metabolism and signal transduction has usually been considered independent processes. Interestingly mitochondria is an intracellular organelle that perform energy production to fuel the cell to carry out its normal functions, however, in certain circumstances, its components can also carry out programmed cell destruction via its resident proteins. In this review, the role of mitochondria and its component proteins in inducing apoptotic programmed cell death is discussed. The role of Bcl-2 family proteins that set up the mitochondria induced apoptotic threshold is also described. Further, how the metabolic stress leads to mitochondrial dysfunction via increased generation of reactive oxygen species are discussed. This article is a part of a special issue on mitochondria summarizes the induction of intracellular pathways that converge on mitochondria and ultimately impact the success of chemotherapeutic interventions.
Published in |
Cell Biology (Volume 3, Issue 2-1)
This article belongs to the Special Issue Mitochondria: Implications in Human Health and Diseases |
DOI | 10.11648/j.cb.s.2015030201.13 |
Page(s) | 17-21 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2015. Published by Science Publishing Group |
Mitochondria, Cancer, Apoptosis, Programmed Cell Death
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APA Style
Ashutosh Shrivastava. (2015). The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy. Cell Biology, 3(2-1), 17-21. https://doi.org/10.11648/j.cb.s.2015030201.13
ACS Style
Ashutosh Shrivastava. The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy. Cell Biol. 2015, 3(2-1), 17-21. doi: 10.11648/j.cb.s.2015030201.13
AMA Style
Ashutosh Shrivastava. The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy. Cell Biol. 2015;3(2-1):17-21. doi: 10.11648/j.cb.s.2015030201.13
@article{10.11648/j.cb.s.2015030201.13, author = {Ashutosh Shrivastava}, title = {The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy}, journal = {Cell Biology}, volume = {3}, number = {2-1}, pages = {17-21}, doi = {10.11648/j.cb.s.2015030201.13}, url = {https://doi.org/10.11648/j.cb.s.2015030201.13}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.s.2015030201.13}, abstract = {Cell metabolism and signal transduction has usually been considered independent processes. Interestingly mitochondria is an intracellular organelle that perform energy production to fuel the cell to carry out its normal functions, however, in certain circumstances, its components can also carry out programmed cell destruction via its resident proteins. In this review, the role of mitochondria and its component proteins in inducing apoptotic programmed cell death is discussed. The role of Bcl-2 family proteins that set up the mitochondria induced apoptotic threshold is also described. Further, how the metabolic stress leads to mitochondrial dysfunction via increased generation of reactive oxygen species are discussed. This article is a part of a special issue on mitochondria summarizes the induction of intracellular pathways that converge on mitochondria and ultimately impact the success of chemotherapeutic interventions.}, year = {2015} }
TY - JOUR T1 - The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy AU - Ashutosh Shrivastava Y1 - 2015/03/12 PY - 2015 N1 - https://doi.org/10.11648/j.cb.s.2015030201.13 DO - 10.11648/j.cb.s.2015030201.13 T2 - Cell Biology JF - Cell Biology JO - Cell Biology SP - 17 EP - 21 PB - Science Publishing Group SN - 2330-0183 UR - https://doi.org/10.11648/j.cb.s.2015030201.13 AB - Cell metabolism and signal transduction has usually been considered independent processes. Interestingly mitochondria is an intracellular organelle that perform energy production to fuel the cell to carry out its normal functions, however, in certain circumstances, its components can also carry out programmed cell destruction via its resident proteins. In this review, the role of mitochondria and its component proteins in inducing apoptotic programmed cell death is discussed. The role of Bcl-2 family proteins that set up the mitochondria induced apoptotic threshold is also described. Further, how the metabolic stress leads to mitochondrial dysfunction via increased generation of reactive oxygen species are discussed. This article is a part of a special issue on mitochondria summarizes the induction of intracellular pathways that converge on mitochondria and ultimately impact the success of chemotherapeutic interventions. VL - 3 IS - 2-1 ER -