Skip to main content Accessibility help
×
Hostname: page-component-848d4c4894-wg55d Total loading time: 0 Render date: 2024-05-20T08:00:30.648Z Has data issue: false hasContentIssue false

4 - Mitochondria and Cell Death

from Part I - General Principles of Cell Death

Published online by Cambridge University Press:  07 September 2011

Douglas R. Green
Affiliation:
St. Jude Children's Research Hospital, Memphis, Tennessee
Gavin P. McStay
Affiliation:
Columbia University
Douglas R. Green
Affiliation:
St. Jude Children’s Research Hospital
John C. Reed
Affiliation:
Sanford-Burnham Medical Research Institute, La Jolla, California
Get access

Summary

Introduction

Cell death pathways use genetically encoded and derived components to transduce specific death-inducing signals into a common phenotype associated with death. These signals often include steps that impinge on mitochondria as a means of initiating or amplifying the process. Because mitochondria are organelles that contain unshared lipid and protein components, this makes them ideal targets for specific integration into cell death pathways at defined steps because of the actions of proteins present in the cytosol that target and respond to these unique components. Mitochondria are the site of the cell's major energy-generating system that produces adenosine triphosphate (ATP), used to maintain vital cellular functions. By being involved in these two conflicting processes, a cell ensures that mitochondrial energy generation and cell death are generally exclusive events. This is compatible with cellular fate ensuring shut-down of anabolic processes and favoring dismantling of cellular architecture and function, thus making death proceed in a swift manner. Here we discuss the function of mitochondria in apoptosis and necrosis and how these roles affect other aspects of mitochondrial biology.

Type
Chapter
Information
Apoptosis
Physiology and Pathology
, pp. 37 - 43
Publisher: Cambridge University Press
Print publication year: 2011

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Baines, CP, Kaiser, RA, Purcell, NH, Blair, NS, Osinska, H, Hambleton, MA, Brunskill, EW, Sayen, MR, Gottlieb, RA, Dorn, GW, Robbins, J, Molkentin, JD. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death. Nature 2005, 434:658–62.
Chipuk, JE, Green, DR. Do inducers of apoptosis trigger caspase-independent cell death? Nat Rev Mol Cell Biol 2005, 6:268–75.
Frank, S, Gaume, B, Bergmann-Leitner, ES, Leitner, WW, Robert, EG, Catez, F, Smith, CL, Youle, RJ. The role of dynamin-related protein 1, a mediator of mitochondrial fission, in apoptosis. Dev Cell 2001, 1:515–25.
Frezza, C, Cipolat, S, Martins de Brito, O, Micaroni, M, Beznoussenko, GV, Rudka, T, Bartoli, D, Polishuck, RS, Danial, NN, De Strooper, B, Scorrano, L. OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. Cell 2006, 126:177–89.
Kluck, RM, Bossy-Wetzel, E, Green, DR, Newmeyer, DD. The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis. Science 1997, 275:1132–6.
Liu, X, Kim, CN, Yang, J, Jemmerson, R, Wang, X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell 1996, 86:147–57.
Ow, YP, Green, DR, Hao, Z, Mak, TW. Cytochrome c: functions beyond respiration. Nat Rev Mol Cell Biol 2008, 9:532–42.
Suen, DF, Norris, KL, Youle, RJ. Mitochondrial dynamics and apoptosis. Genes Dev 2008, 22:1577–90.
Wang, C, Youle, RJ. The role of mitochondria in apoptosis. Annu Rev Genet 2009, 43:95–118.
Youle, RJ, Strasser, A. The BCL-2 protein family: opposing activities that mediate cell death. Nat Rev Mol Cell Biol 2008, 9:47–59.

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×