Abstract
The vascular endothelial growth factor (VEGF) family, the crucial regulator of angiogenesis, lymphangiogenesis, lipid metabolism and inflammation, is involved in the development of atherosclerosis and further CVDs (cardiovascular diseases). This review discusses the general regulation and functions of VEGFs, their role in lipid metabolism and atherosclerosis development and progression. These functions present the great potential of applying the VEGF family as a target in the treatment of atherosclerosis and related CVDs. In addition, we discuss several modern anti-atherosclerosis VEGFs-targeted experimental procedures, drugs and natural compounds, which could significantly improve the efficiency of atherosclerosis and related CVDs’ treatment.
Highlights
The vascular endothelial growth factor (VEGF) is a family of heparin-binding proteins involved in angiogenesis, lymphopoiesis and lymphangiogenesis, resisting oxidative stress, regulation of lipid metabolism and inflammation
VEGF family consists of 5 gene products in humans, 3 of which regulate blood vessel growth (VEGF-A, VEGF-B and PlGF, and 2 modulate lymphangiogenesis (VEGF-C and VEGF-D)
Paeoniflorin (PF) both could alleviate atherosclerosis [81,82]. As it was shown on ox-LDL induced HUVECs angiogenesis, TMP and PF treatment inhibited VEGF and VEGFR2 expression and decreased expression of angiogenesisrelated factors Notch1 (NOTCH1), Jagged1 (JAG1), and Hes1 (HES1), which might contribute to the stability of plaques in atherosclerosis [83]
Summary
The VEGF is a family of heparin-binding proteins involved in angiogenesis, lymphopoiesis and lymphangiogenesis, resisting oxidative stress, regulation of lipid metabolism and inflammation. The VEGF family can inhibit the inflammatory response, promote dilation and proliferation of lymphatic vessels and reduce oxidative stress, prevent atherosclerosis progress [5]. VEGF signalling is involved in the regulation of ECs survival and adaptation to ER-stress via activation of UPRER (unfolded protein response) mediators through a Phospholipase C Gamma 1-mediated crosstalk with the mTORC1 Kinase contributes to the survival effect of VEGF on ECs (endothelial cells) by positively regulating mTORC2-mediated phosphorylation of AKT We briefly discuss every member of the VEGF family, their general functions, regulation, role in lipid metabolism and in atherosclerosis development and progression. The role of VEGF in cancer development and treatment is far beyond the focus of this review, and we wish to redirect interested readers to cited papers [6,7,9]
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