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Open AccessJournal ArticleDOI

Programmed cell deaths

Cinthya A. Guimarães, +1 more
- 01 May 2004 - 
- Vol. 271, Iss: 9, pp 1638-1650
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TLDR
Increasing evidence obtained both in vitro and in vivo supports the hypothesis that a variety of cell death programs may be triggered in distinct circumstances, and the view that caspase-mediated apoptosis represents the standard programmed cell death is challenged.
Abstract
Programmed cell death is a major component of both normal development and disease. The roles of cell death during either embryogenesis or pathogenesis, the signals that modulate this event, and the mechanisms of cell demise are the major subjects that drive research in this field. Increasing evidence obtained both in vitro and in vivo supports the hypothesis that a variety of cell death programs may be triggered in distinct circumstances. Contrary to the view that caspase-mediated apoptosis represents the standard programmed cell death, recent studies indicate that an apoptotic morphology can be produced independent of caspases, that autophagic execution pathways of cell death may be engaged without either the involvement of caspases or morphological signs of apoptosis, and that even the necrotic morphology of cell death may be consistently produced in some cases, including certain plants. Alternative cell death programs may imply novel therapeutic targets, with important consequences for attempts to treat diseases associated with disregulated programmed cell death.

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Citations
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Overview of cell death signaling pathways

TL;DR: Changing attention is being focused on alternative signaling pathways leading to cell death including necrosis, autophagy, and mitotic catastrophe.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Oxidative Stress and Autophagy

TL;DR: Recent evidence supports a protective role of the lysosomal system, which can eliminate altered intracellular components through autophagy, at least in the first stages of oxidative injury.
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Mitochondrial electron-transport-chain inhibitors of complexes I and II induce autophagic cell death mediated by reactive oxygen species.

TL;DR: Results indicate that targeting mETC complex I and II selectively induces autophagic cell death through a ROS-mediated mechanism, and treatment of non-transformed primary mouse astrocytes with rotenone or TTFA failed to significantly increase levels of ROS or autophagy.
References
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Journal ArticleDOI

Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.

TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
Journal ArticleDOI

Mitochondria and apoptosis

TL;DR: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins.
Book ChapterDOI

Cell death : the significance of apoptosis

TL;DR: It has proved feasible to categorize most if not all dying cells into one or the other of two discrete and distinctive patterns of morphological change, which have, generally, been found to occur under disparate but individually characteristic circumstances.
Journal ArticleDOI

The biochemistry of apoptosis

TL;DR: The basic components of the death machinery are reviewed, how they interact to regulate apoptosis in a coordinated manner is described, and the main pathways that are used to activate cell death are discussed.
Journal ArticleDOI

Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
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