Figure 1.

The crosstalk between PVAT and the vessel wall modulates vascular functions. PVAT releases vasoactive molecules, hormones, adipokines, and microvesicles. PVAT-derived relaxing factors (PVRFs) include leptin and adiponectin, hydrogen sulphide (H₂S), hydrogen peroxide (H₂O₂), prostaglandins, NO, and angiotensin (Ang) 1–7. PVAT-derived contracting factors (PVCFs) include chemerin, calpastatin, 5-hydroxytryptamine (5-HT), norepinephrine (NE), AngII, and ROS. These factors from PVAT may reach the endothelial layer of blood vessels by either direct diffusion or via vasa vasorum or small media conduit networks connecting the medial layer with the underlying adventitia and modulate vasodilation and vasocontraction. PVAT plays a critical role in vascular homeostasis via secreting adipokine, hormones, and growth factors to modulate the proliferation of VSMCs. Adipocytes from PVAT also secrete different types of extracellular vesicles, including exosomes and microvesicles, which have also been shown to trigger early vascular remodeling in vascular inflammation. Under pathological conditions, PVAT becomes dysfunctional, and the secretion of the PVAT-derived factor becomes imbalanced which could exert detrimental effects on vascular homeostasis and lead to vascular remodeling and arterial stiffening.