Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease
UMass Chan Affiliations
Department of Molecular, Cell and Cancer BiologyDocument Type
Journal ArticlePublication Date
2017-08-01Keywords
apoptosiscaspases
apoptosis-induced proliferation
Cell Biology
Cellular and Molecular Physiology
Metadata
Show full item recordAbstract
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.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 siteDOI
10.1038/cdd.2017.47Permanent Link to this Item
http://hdl.handle.net/20.500.14038/40303PubMed ID
28362431Related Resources
Rights
Copyright The Author(s) 2017Distribution License
http://creativecommons.org/licenses/by-nc-nd/4.0/ae974a485f413a2113503eed53cd6c53
10.1038/cdd.2017.47