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Cited by 471

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Control of apoptosis by the cellular ATP level

Open access
Richter, Christoph, Schweizer, Matthias, Cossarizza, Andrea, Franceschi, Claudio·1996·FEBS Letters

Abstract

Apoptosis is a physiological form of cell death. Its causes and execution mechanisms are not clearly understood. Oxidative stress, nitric oxide and its congeners, Ca 2+, proteases, nucleases, and mitochondria are considered mediators of apoptosis. At present their importance and exact role are elusive but it is clear that mitochondria are both the target and the source of oxidative stress, nitric oxide, and Ca 2+. The mitochondrial membrane potential (ΔΨ), which is the driving force for mitochondrial ATP synthesis, declines during apoptosis, and maintenance of ΔΨ prevents apoptosis. Since apoptosis is highly regulated and involves the activity of hydrolytic enzymes, chromatin condensation and vesicle formation apoptosis is likely to have a high energy demand. We propose that the cellular ATP level is an important determinant for cell death. This hypothesis is supported by circumstantial evidence, is consistent with the available data, has a corrolary in aging, and is amenable to direct experimental testing particularly with flow cytometry as a promising tool.

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Crossref · 10.1016/0014-5793(95)01431-4

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Metadata

Authors
Richter, C., Schweizer, M., Cossarizza, A., & Franceschi, C.
Venue
FEBS Letters
Publisher
Wiley
Published
1996-01-08
Volume
378
Issue
2
Pages
107-110
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W1972440163
Cited by
471
References
1
FWCI
15.09
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Control of apoptosis by the cellular ATP level. https://app.cochat.ai/papers/10.1016/0014-5793(95)01431-4
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Richter, C., Schweizer, M., Cossarizza, A., & Franceschi, C. (1996). Control of apoptosis by the cellular ATP level. FEBS Letters. https://doi.org/10.1016/0014-5793(95)01431-4

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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