The Role and Therapeutic Potential of Autophagy Modulation in Controlling Virus-Induced Cell Death
2014
Autori:
Tovilović-Kovačević, GordanaRistić, Biljana
Milenković, Marina
Stanojević, Maja
Trajković, Vladimir
Tip dokumenta:
Članak u časopisu (Objavljena verzija)
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© 2013 Wiley Periodicals, Inc.
Metapodaci
Prikaz svih podataka o dokumentuApstrakt:
Macroautophagy (hereafter referred to as autophagy) is an evolutionary conserved catabolic process in which the cytoplasmic content is sequestered and degraded by the lysosomal machinery in order to maintain cellular homeostasis or provide energy during metabolic and hypoxic stress. It also represents an important component of the host response against infectious agents, performing surveillance and effector functions involved in detection and clearance of pathogens, including viruses. Moreover, it appears that autophagy plays a major role in determining the fate of both virally infected and uninfected cells by blocking or promoting their death in a virus- and cell-type-dependent manner. We here review the current knowledge on the complex involvement of autophagy in survival and death of the host cells during viral infection, focusing on the molecular mechanisms underlying viral modulation of autophagic response and its interference with the cell death pathways. We also discuss a possible significance of the autophagy-dependent modulation of cell death for the outcome and therapy of viral infections, emphasizing the need for a time- and cell-type-dependent fine-tuning of the autophagic response in achieving an optimal balance between beneficial and adverse effects.
Ključne reči:
autophagy; virus; cell death; apoptosis; therapyIzvor:
Medicinal Research Reviews, 2014, 34, 4, 744-767Finansiranje / projekti:
- Fizičke osnove primene neravnotežnih plazmi u nanotehnologijama i tretmanu materijala (RS-MESTD-MPN2006-2010-141025)
- Filogenetski pristup analizi molekularne evolucije visoko varijabilnih virusa - koinfekcije, interakcija virusa i domaćina (RS-MESTD-Basic Research (BR or ON)-175024)
DOI: 10.1002/med.21303
ISSN: 0198-6325
PubMed: 24123125