Visfatin/Nampt: An Adipokine with Cardiovascular Impact

Table 2

Direct vascular proinflammatory actions of visfatin and their proposed underlying mechanisms.

Target cell type	Cellular actions	Mechanism of action	References
Smooth muscle cells	ERK 1/2-NF-𝜅B activation; iNOS induction	Nampt activity,; insulin receptor independent	[96]
Endothelial cells	NF-𝜅B activation	Insulin receptor independent	[82, 84, 97]
	IL-6, IL-8 release	N.D.	[84, 98]
	MCP-1 release	N.D.	[82, 98]
	CCR2 expression	N.D.	[82]
	ICAM-1, VCAM-1, and E-selectin	Insulin receptor independent	[84, 97]
	induction
	MMP-2 and MMP-9 activation	N.D.	[99]
	NADPH oxidase activation	Nampt activity (HUVEC)	[100]
		Lipid rafts (BCAEC and GEC)	[101, 102]
Monocytes	Binding to endothelial cells	N.D.	[84]
	MMP-9 activation	Insulin receptor independent	[63]
Macrophages	Cell survival	STAT3/IL-6 release Nampt- and insulin receptor-independent	[95]
	Lipid accumulation	SR-A, CD36 activation	[103]
Peripheral blood mononuclear cells	Cytokine release (IL-8, TNF-𝛼)	Insulin receptor	[63]

N.D.: not determined. BCAEC: bovine coronary artery endothelial cells, CCR2: chemokine receptor type 2, CD36: cluster of differentiation 36, ERK 1/2: extracellular signal-regulated kinase 1/2, GEC: glomerular endotelial cells, HUVEC: human umbilical vein endothelial cells, ICAM-1: intercellular adhesion molecule-1, IL: interleukin, MCP-1: monocyte chemotactic protein-1, MMP: matrix metalloproteinase, NF-𝜅B: nuclear factor-𝜅B, iNOS: inducible nitric oxide synthase, SR-A: scavenger receptor-A, STAT3: signal transducer and activator of transcription 3, TNF-𝛼: tumor necrosis factor-𝛼, and VCAM-1: vascular cell adhesion molecule-1.