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A Vectorial, ER-Mitochondria Link to Energy Homeostasis in the Vascular Endothelium

Authors
  • Boutagy, Nabil E.1, 2
  • Fowler, Joseph W.1, 2
  • Sessa, William C.1, 2, 3
  • 1 Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut, USA
  • 2 Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, Connecticut, USA
  • 3 Department of Cardiology, Yale University School of Medicine, New Haven, Connecticut, USA
Type
Published Article
Journal
Cell metabolism
Publication Date
Aug 04, 2020
Volume
32
Issue
2
Pages
150–152
Identifiers
DOI: 10.1016/j.cmet.2020.07.010
PMID: 32755606
PMCID: PMC7652390
Source
PubMed Central
Disciplines
  • Article
License
Unknown

Abstract

The precise mechanisms of free fatty acid (FFA) uptake in the vascular endothelium are unclear. This study used a high-throughput screen of chemicals that may impact FFA uptake and transport in human endothelial cell (ECs) cultures. Niclosamide was identified as a rapid and potent inhibitor of FFA in ECs. Further metabolic and biochemical characterization led to the discovery that FFA uptake was partially mediated by mitochondrial ATP production that was used locally for the acyl-CoA synthetase activity of the ER-located fatty acid transport protein 4. This data support provides the first evidence of a vectorial, ER-mitochondria link to energy homeostasis in the vascular endothelium

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