G protein-coupled receptors and the regulation of autophagy

Eric M. Wauson, Hashem A. Dbouk, Anwesha B. Ghosh, Melanie H. Cobb

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)274-282
Number of pages9
JournalTrends in Endocrinology and Metabolism
Volume25
Issue number5
DOIs
StatePublished - 2014

Fingerprint

Autophagy
G-Protein-Coupled Receptors
Food
Organelles
Neurotransmitter Agents
Hormones
Pharmaceutical Preparations

Keywords

  • Amino acid sensing GPCRs
  • AMPK
  • Autophagy
  • GLP-1 receptor
  • MTORC1
  • Muscarinic receptor
  • β-adrenergic receptor

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Medicine(all)

Cite this

G protein-coupled receptors and the regulation of autophagy. / Wauson, Eric M.; Dbouk, Hashem A.; Ghosh, Anwesha B.; Cobb, Melanie H.

In: Trends in Endocrinology and Metabolism, Vol. 25, No. 5, 2014, p. 274-282.

Research output: Contribution to journalArticle

Wauson, Eric M. ; Dbouk, Hashem A. ; Ghosh, Anwesha B. ; Cobb, Melanie H. / G protein-coupled receptors and the regulation of autophagy. In: Trends in Endocrinology and Metabolism. 2014 ; Vol. 25, No. 5. pp. 274-282.
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