VEGF-A in Cardiomyocytes and Heart Diseases
Department of Translational Medical Sciences and Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, 80131 Naples, Italy
WAO Center of Excellence, 80131 Naples, Italy
CNR Institute of Experimental Endocrinology and Oncology “G. Salvatore”, 80131 Naples, Italy
Department of Public Health, University of Naples Federico II, 80131 Naples, Italy
Azienda Ospedaliera Ospedali dei Colli – Monaldi Hospital Pharmacy, 80131 Naples, Italy
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(15), 5294; https://doi.org/10.3390/ijms21155294
Received: 8 June 2020 / Revised: 21 July 2020 / Accepted: 22 July 2020 / Published: 26 July 2020
(This article belongs to the Special Issue Mechanisms of Inflammation in Degenerative Cardiovascular Conditions 2.0)
The vascular endothelial growth factor (VEGF), a homodimeric vasoactive glycoprotein, is the key mediator of angiogenesis. Angiogenesis, the formation of new blood vessels, is responsible for a wide variety of physio/pathological processes, including cardiovascular diseases (CVD). Cardiomyocytes (CM), the main cell type present in the heart, are the source and target of VEGF-A and express its receptors, VEGFR1 and VEGFR2, on their cell surface. The relationship between VEGF-A and the heart is double-sided. On the one hand, VEGF-A activates CM, inducing morphogenesis, contractility and wound healing. On the other hand, VEGF-A is produced by CM during inflammation, mechanical stress and cytokine stimulation. Moreover, high concentrations of VEGF-A have been found in patients affected by different CVD, and are often correlated with an unfavorable prognosis and disease severity. In this review, we summarized the current knowledge about the expression and effects of VEGF-A on CM and the role of VEGF-A in CVD, which are the most important cause of disability and premature death worldwide. Based on clinical studies on angiogenesis therapy conducted to date, it is possible to think that the control of angiogenesis and VEGF-A can lead to better quality and span of life of patients with heart disease.