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Autophagy: for better or for worse

Ellen Wirawan UGent, Tom Vanden Berghe UGent, Saskia Lippens UGent, Patrizia Agostinis and Peter Vandenabeele UGent (2012) CELL RESEARCH. 22(1). p.43-61
abstract
Autophagy is a lysosomal degradation pathway that degrades damaged or superfluous cell components into basic biomolecules, which are then recycled back into the cytosol. In this respect, autophagy drives a flow of biomolecules in a continuous degradation-regeneration cycle. Autophagy is generally considered a pro-survival mechanism protecting cells under stress or poor nutrient conditions. Current research clearly shows that autophagy fulfills numerous functions in vital biological processes. It is implicated in development, differentiation, innate and adaptive immunity, ageing and cell death. In addition, accumulating evidence demonstrates interesting links between autophagy and several human diseases and tumor development. Therefore, autophagy seems to be an important player in the life and death of cells and organisms. Despite the mounting knowledge about autophagy, the mechanisms through which the autophagic machinery regulates these diverse processes are not entirely understood. In this review, we give a comprehensive overview of the autophagic signaling pathway, its role in general cellular processes and its connection to cell death. In addition, we present a brief overview of the possible contribution of defective autophagic signaling to disease.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
vesicle, autophagosome, autophagy, degradation, cell death, PROGRAMMED CELL-DEATH, BECLIN 1-DEPENDENT AUTOPHAGY, ENDOGENOUS VIRAL-ANTIGENS, INNATE IMMUNE-RESPONSE, LIFE-SPAN EXTENSION, COLON-CANCER CELLS, MICROSATELLITE INSTABILITY, MITOCHONDRIAL CLEARANCE, ENDOPLASMIC-RETICULUM, MEDIATED AUTOPHAGY
journal title
CELL RESEARCH
Cell Res.
volume
22
issue
1
pages
43 - 61
Web of Science type
Review
Web of Science id
000299312900009
JCR category
CELL BIOLOGY
JCR impact factor
10.526 (2012)
JCR rank
18/181 (2012)
JCR quartile
1 (2012)
ISSN
1001-0602
DOI
10.1038/cr.2011.152
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2034560
handle
http://hdl.handle.net/1854/LU-2034560
date created
2012-02-16 09:44:44
date last changed
2014-05-12 10:58:43
@article{2034560,
  abstract     = {Autophagy is a lysosomal degradation pathway that degrades damaged or superfluous cell components into basic biomolecules, which are then recycled back into the cytosol. In this respect, autophagy drives a flow of biomolecules in a continuous degradation-regeneration cycle. Autophagy is generally considered a pro-survival mechanism protecting cells under stress or poor nutrient conditions. Current research clearly shows that autophagy fulfills numerous functions in vital biological processes. It is implicated in development, differentiation, innate and adaptive immunity, ageing and cell death. In addition, accumulating evidence demonstrates interesting links between autophagy and several human diseases and tumor development. Therefore, autophagy seems to be an important player in the life and death of cells and organisms. Despite the mounting knowledge about autophagy, the mechanisms through which the autophagic machinery regulates these diverse processes are not entirely understood. In this review, we give a comprehensive overview of the autophagic signaling pathway, its role in general cellular processes and its connection to cell death. In addition, we present a brief overview of the possible contribution of defective autophagic signaling to disease.},
  author       = {Wirawan, Ellen and Vanden Berghe, Tom and Lippens, Saskia and Agostinis, Patrizia and Vandenabeele, Peter},
  issn         = {1001-0602},
  journal      = {CELL RESEARCH},
  keyword      = {vesicle,autophagosome,autophagy,degradation,cell death,PROGRAMMED CELL-DEATH,BECLIN 1-DEPENDENT AUTOPHAGY,ENDOGENOUS VIRAL-ANTIGENS,INNATE IMMUNE-RESPONSE,LIFE-SPAN EXTENSION,COLON-CANCER CELLS,MICROSATELLITE INSTABILITY,MITOCHONDRIAL CLEARANCE,ENDOPLASMIC-RETICULUM,MEDIATED AUTOPHAGY},
  language     = {eng},
  number       = {1},
  pages        = {43--61},
  title        = {Autophagy: for better or for worse},
  url          = {http://dx.doi.org/10.1038/cr.2011.152},
  volume       = {22},
  year         = {2012},
}

Chicago
Wirawan, Ellen, Tom Vanden Berghe, Saskia Lippens, Patrizia Agostinis, and Peter Vandenabeele. 2012. “Autophagy: For Better or for Worse.” Cell Research 22 (1): 43–61.
APA
Wirawan, E., Vanden Berghe, T., Lippens, S., Agostinis, P., & Vandenabeele, P. (2012). Autophagy: for better or for worse. CELL RESEARCH, 22(1), 43–61.
Vancouver
1.
Wirawan E, Vanden Berghe T, Lippens S, Agostinis P, Vandenabeele P. Autophagy: for better or for worse. CELL RESEARCH. 2012;22(1):43–61.
MLA
Wirawan, Ellen, Tom Vanden Berghe, Saskia Lippens, et al. “Autophagy: For Better or for Worse.” CELL RESEARCH 22.1 (2012): 43–61. Print.