Journal
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 25, Issue 5, Pages 274-282Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2014.03.006
Keywords
autophagy; amino acid sensing GPCRs; muscarinic receptor; beta-adrenergic receptor; GLP-1 receptor; mTORC1; AMPK
Categories
Funding
- National Institutes of Health [R01 DK55310]
- Cancer Prevention and Research Institute of Texas (CPRIT)
- American Diabetes Association
Ask authors/readers for more resources
Autophagy is an important catabolic cellular process that eliminates damaged and unnecessary cytoplasmic proteins and organelles. Basal autophagy occurs during normal physiological conditions, but the activity of this process can be significantly altered in human diseases. Thus, defining the regulatory inputs and signals that control autophagy is essential. Nutrients are key modulators of autophagy. Although autophagy is generally accepted to be regulated in a cell-autonomous fashion, recent studies suggest that nutrients can modulate autophagy in a systemic manner by inducing the secretion of hormones and neurotransmitters that regulate G protein-coupled receptors (GPCRs). Emerging studies show that GPCRs also regulate autophagy by directly detecting extracellular nutrients. We review the role of GPCRs in autophagy regulation, highlighting their potential as therapeutic drug targets.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available