An unexpected friend − ROS in apoptosis-induced compensatory proliferation: Implications for regeneration and cancer

Apoptosis-induced compensatory proliferation (AiP) is a form of compensatory proliferation that is triggered by apoptotic cell death to maintain tissue homeostasis. As such, AiP is essential for many tissue repair processes including regeneration. The apoptotic effectors, termed caspases, not only e...

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Bibliographic Details
Published inSeminars in cell & developmental biology Vol. 80; pp. 74 - 82
Main Authors Diwanji, Neha, Bergmann, Andreas
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.08.2018
Subjects
Animals
Apoptosis - physiology
Apoptosis-induced proliferation
Cell Proliferation - physiology
Drosophila
Humans
Macrophages
Neoplasms - metabolism
Reactive oxygen species
Reactive Oxygen Species - metabolism
Regeneration
Regeneration - physiology
Signal Transduction - physiology
Regeneration
Reactive oxygen species
Apoptosis-induced proliferation
Macrophages
Drosophila
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Summary:Apoptosis-induced compensatory proliferation (AiP) is a form of compensatory proliferation that is triggered by apoptotic cell death to maintain tissue homeostasis. As such, AiP is essential for many tissue repair processes including regeneration. The apoptotic effectors, termed caspases, not only execute apoptosis, but are also directly involved in the generation of the signals required for AiP. Reactive oxygen species (ROS) play an important role for regenerative processes. Recently, it was shown in Drosophila that apoptotic caspases can mediate the generation of ROS for promoting AiP. This review summarizes and discusses these findings in the context of regenerative processes and cancer.
Bibliography:ObjectType-Article-2
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ISSN:1084-9521
1096-3634
DOI:10.1016/j.semcdb.2017.07.004