Format

Send to

Choose Destination
Trends Mol Med. 2019 Aug;25(8):723-734. doi: 10.1016/j.molmed.2019.05.010. Epub 2019 Jun 21.

ANGPTL4 in Metabolic and Cardiovascular Disease.

Author information

1
Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Yale University School of Medicine, New Haven, CT, USA; Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA. Electronic address: binod.aryal@yale.edu.
2
Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Yale University School of Medicine, New Haven, CT, USA; Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA.
3
Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Yale University School of Medicine, New Haven, CT, USA; Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
4
Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Yale University School of Medicine, New Haven, CT, USA; Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT, USA. Electronic address: carlos.fernandez@yale.edu.

Abstract

Alterations in circulating lipids and ectopic lipid deposition impact on the risk of developing cardiovascular and metabolic diseases. Lipoprotein lipase (LPL) hydrolyzes fatty acids (FAs) from triglyceride (TAG)-rich lipoproteins including very low density lipoproteins (VLDLs) and chylomicrons, and regulates their distribution to peripheral tissues. Angiopoietin-like 4 (ANGPTL4) mediates the inhibition of LPL activity under different circumstances. Accumulating evidence associates ANGPTL4 directly with the risk of atherosclerosis and type 2 diabetes (T2D). This review focuses on recent findings on the role of ANGPTL4 in metabolic and cardiovascular diseases. We highlight human and murine studies that explore ANGPTL4 functions in different tissues and how these effect disease development through possible autocrine and paracrine forms of regulation.

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center