UMMS Affiliation

Department of Molecular, Cell and Cancer Biology

Publication Date

8-1-2017

Document Type

Article

Disciplines

Cell Biology | Cellular and Molecular Physiology

Abstract

Apoptosis is a carefully orchestrated and tightly controlled form of cell death, conserved across metazoans. As the executioners of apoptotic cell death, cysteine-dependent aspartate-directed proteases (caspases) are critical drivers of this cellular disassembly. Early studies of genetically programmed cell death demonstrated that the selective activation of caspases induces apoptosis and the precise elimination of excess cells, thereby sculpting structures and refining tissues. However, over the past decade there has been a fundamental shift in our understanding of the roles of caspases during cell death-a shift precipitated by the revelation that apoptotic cells actively engage with their surrounding environment throughout the death process, and caspases can trigger a myriad of signals, some of which drive concurrent cell proliferation regenerating damaged structures and building up lost tissues. This caspase-driven compensatory proliferation is referred to as apoptosis-induced proliferation (AiP). Diverse mechanisms of AiP have been found across species, ranging from planaria to mammals. In this review, we summarize the current knowledge of AiP and we highlight recent advances in the field including the involvement of reactive oxygen species and macrophage-like immune cells in one form of AiP, novel regulatory mechanisms affecting caspases during AiP, and emerging clinical data demonstrating the critical importance of AiP in cancer.

Rights and Permissions

Copyright The Author(s) 2017

DOI of Published Version

10.1038/cdd.2017.47

Source

Cell Death Differ. 2017 Aug;24(8):1390-1400. doi: 10.1038/cdd.2017.47. Epub 2017 Mar 31. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Keywords

apoptosis, caspases, apoptosis-induced proliferation

Journal/Book/Conference Title

Cell death and differentiation

PubMed ID

28362431

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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