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J Exp Med. 2015 Jun 29;212(7):979-90. doi: 10.1084/jem.20150956. Epub 2015 Jun 22.

Therapeutic targeting of autophagy in neurodegenerative and infectious diseases.

Author information

1
Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Cambridge CB2 OSP, England, UK dcr1000@cam.ac.uk vderetic@salud.unm.edu.
2
Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Cambridge CB2 OSP, England, UK.
3
Department of Molecular Genetics and Microbiology and Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 Department of Molecular Genetics and Microbiology and Department of Neurology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 dcr1000@cam.ac.uk vderetic@salud.unm.edu.

Abstract

Autophagy is a conserved process that uses double-membrane vesicles to deliver cytoplasmic contents to lysosomes for degradation. Although autophagy may impact many facets of human biology and disease, in this review we focus on the ability of autophagy to protect against certain neurodegenerative and infectious diseases. Autophagy enhances the clearance of toxic, cytoplasmic, aggregate-prone proteins and infectious agents. The beneficial roles of autophagy can now be extended to supporting cell survival and regulating inflammation. Autophagic control of inflammation is one area where autophagy may have similar benefits for both infectious and neurodegenerative diseases beyond direct removal of the pathogenic agents. Preclinical data supporting the potential therapeutic utility of autophagy modulation in such conditions is accumulating.

PMID:
26101267
PMCID:
PMC4493419
DOI:
10.1084/jem.20150956
[Indexed for MEDLINE]
Free PMC Article

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