The molecular machinery of regulated cell death

被引:0
|
作者
Daolin Tang
Rui Kang
Tom Vanden Berghe
Peter Vandenabeele
Guido Kroemer
机构
[1] Guangzhou Medical University,The Third Affiliated Hospital, Protein Modification and Degradation Lab, School of Basic Medical Sciences
[2] UT Southwestern Medical Center,Department of Surgery
[3] Flanders Institute for Biotechnology,Molecular Signaling and Cell Death Unit, VIB
[4] Ghent University,UGent Center for Inflammation Research
[5] University of Antwerp,Department for Biomedical Molecular Biology
[6] Ghent University,Laboratory of Pathophysiology, Faculty of Biomedical Sciences
[7] Université Paris Descartes,Methusalem program
[8] Sorbonne Paris Cité,Department of Women’s and Children’s Health
[9] Equipe 11 labellisée Ligue Nationale contre le Cancer,undefined
[10] Centre de Recherche des Cordeliers,undefined
[11] Institut National de la Santé et de la Recherche Médicale,undefined
[12] Université Pierre et Marie Curie,undefined
[13] Metabolomics and Cell Biology Platforms,undefined
[14] Gustave Roussy Cancer Campus,undefined
[15] Pôle de Biologie,undefined
[16] Hôpital Européen Georges Pompidou,undefined
[17] AP-HP,undefined
[18] Karolinska University Hospital,undefined
来源
Cell Research | 2019年 / 29卷
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摘要
Cells may die from accidental cell death (ACD) or regulated cell death (RCD). ACD is a biologically uncontrolled process, whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms. A growing number of novel non-apoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies. Here, we critically review the current state of the art regarding non-apoptotic types of RCD, including necroptosis, pyroptosis, ferroptosis, entotic cell death, netotic cell death, parthanatos, lysosome-dependent cell death, autophagy-dependent cell death, alkaliptosis and oxeiptosis. The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidance of pathogenic cell loss.
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页码:347 / 364
页数:17
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