Role of the fatty acid-binding protein 4 in heart failure and cardiovascular disease
- Ricardo Rodríguez-Calvo1⇑,
- Josefa Girona1,
- Josep M Alegret2,
- Alba Bosquet1,
- Daiana Ibarretxe1 and
- Lluís Masana1
- 1Vascular Medicine and Metabolism Unit, Research Unit on Lipids and Atherosclerosis, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Reus, Spain
- 2Department of Cardiology, Cardiovascular Research Group, ‘Sant Joan’ University Hospital, Universitat Rovira i Virgili, Institut de Investigació Sanitaria Pere Virgili (IISPV), Reus, Spain
- Correspondence should be addressed to R Rodríguez-Calvo; Email: ricardo.rodriguez{at}ciberdem.org
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Figure 1
Three-dimensional structure of human FABP4 complexed with palmitic acid. The 10-stranded anti-parallel β-barrel structure of FABP4 is shown. The bound palmitic acid in the pocket of the β-barrel structure is shown. The images were rendered from the PDB file 2HNX, which contains the crystal structure of human FABP4. A full colour version of this figure is available at http://dx.doi.org/10.1530/JOE-17-0031.
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Figure 2
Endocrine and paracrine effects of FABP4 linked to obesity-induced HF and CVD. Both visceral and cardiac fat accumulation are important sources of FABP4, which is released into the bloodstream and targets several organs, including the heart. Additionally, macrophages and cardiomyocytes are relevant producers of FABP4. FABP4 is associated with coronary atherosclerosis, the number of stenotic coronary arteries, increased carotid intima-media thickness and ischaemic stroke. FABP4 exerts a cardiodepressant effect and has directly been linked to LVH and LV dysfunction. Thus, FABP4 directly contributes to CVD and HF development. A full colour version of this figure is available at http://dx.doi.org/10.1530/JOE-17-0031.
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Figure 3
Cardiac transendothelial FA transport is regulated by FABP4. Endothelial cells are also an important source of FABP4, which increases transendothelial transport of FAs to the surrounding tissues including the heart. Given the sensitivity of cardiomyocytes in the use of FAs as an energy substrate, this may be one of the potential mechanisms by which FABP4 contributes to the dysregulation of cardiac metabolism and myocardial function. A full colour version of this figure is available at http://dx.doi.org/10.1530/JOE-17-0031.
- © 2017 Society for Endocrinology
