Table 1.

Central roles of PVAT inflammation in vascular diseases.

	Vessels	PVAT	Reference
Vascular aging	Increased tunica media thickness Increased oxidative stress and inflammation (ET-1, iNOS, COX2) VSMCs proliferation Increased perivascular fibrosis Increased arterial stiffness	PVAT was hypertrophic and the average area of single adipocyte was significantly increased The differentiation ability of PVASCs decreased Increased proinflammatory mediators (TNF-α, IL-6, eotaxin, MIP-1α, MCP-1 and RANTES) Reduction of ant-inflammatory mediators (APN) The function of anti- vasoconstriction is weakened The infiltration of macrophages and natural killer cells	(59–68)
Atherosclerosis	The infiltration of macrophages, T cells and dendritic cells increased Plaque volume increased, internal lipid increased, high macrophage density and fibrin deposition Increased proinflammatory mediators Increased perivascular inflammation	The size of adipocytes was smaller and the differentiation phenotype was less Increased proinflammatory mediators (TNF-α, IL-6, IL-1β, MCP-1, resistin, and osteoprotegerin) Reduction of ant-inflammatory mediators (APN) The infiltration of macrophages, T cells and dendritic cells increased B-1 cells and their secretion of anti-atherosclerotic IgM decrease	(10, 18, 69–77) (67, 78–86)
Hypertension	Increased proinflammatory mediators (MCP-1, RANTES and MIP-1α) Endothelial dysfunction Increased vascular tone Systolic and diastolic blood pressure increased vascular hypertrophy and fibrosis Increased perivascular inflammation	The function of anti- vasoconstriction is weakened Decreased production of vasodilator factor Increased angiotensin II secretion Increased proinflammatory mediators (IFN-γ, RANTES, C3, C5a, MCP-1, TNF-α, IL-6, MIP-1α) Reduction of ant-inflammatory mediators (APN) The infiltration of macrophages, T cells and dendritic cells increased The number of eosinophils decreased	(17, 55, 68, 72, 87–97)
Diabetes mellitus related vascular dysfunction	Increased insulin resistance Impaired vasodilation and vascular remodeling mediated by insulin The adhesion ability of endothelial cells to lymphocytes increased	PVAT phenotype changed to pro-inflammatory, pro oxidative and pro vasoconstrictive state Increased infiltration of M1 macrophages and dendritic cells Overproduction of proinflammatory cytokines(IFN-γ, TNF-α, and IL-6) Reduction of anti-inflammatory cytokines (IL-10 and APN)	(98–102)
Abdominal aortic aneurysm	Recruitment of inflammatory cells (macrophages, lymphocytes, and mast cells) in vascular wall Increased expression of perivascular inflammatory factors Enhanced leukocyte- fibroblast interaction in adventitia Migration and proliferation of adventitial fibroblasts increased	Increased PVAT deposition Co-localization of PVAT inflammation and abdominal aortic aneurysm Increased gene expression of proinflammatory factors (IL-8, PTPRC, LCK, and CCL5) Decreased expression of anti-inflammatory PPARγ	(103–111)

The table lists changes in PVAT and vascular inflammation during the onset of vascular aging, atherosclerosis, hypertension, diabetes mellitus-related vascular dysfunction and abdominal aortic aneurysm (note that the anti-atherosclerotic effects of healthy PVAT are not listed). ET-1, endothelin-1; iNOS, inducible nitric oxide synthase; COX2, cyclooxygenase 2; VSMCs, vascular smooth muscle cells; PVASCs, resident stromal cells in PVAT; APN, adiponectin; PTPRC, protein tyrosine phosphatase receptor type C; LCK, lymphocyte-specific protein tyrosine kinase; PPARγ, peroxisome proliferator-activated receptor gamma.