Abstract
Perivascular adipose tissue (PVAT) surrounds most large blood vessels and plays an important role in vascular homeostasis. PVAT releases various chemokines and adipocytokines, functioning in an endocrine and paracrine manner to regulate vascular signaling and inflammation. Mounting evidence suggests that PVAT plays an important role in atherosclerosis and hypertension; however, the role of PVAT in non-atherosclerotic vascular diseases, including neointimal formation, aortic aneurysm, arterial stiffness and vasculitis, has received far less attention. Increasing evidence suggests that PVAT responds to mechanical endovascular injury and regulates the subsequent formation of neointima via factors that promote smooth muscle cell growth, adventitial inflammation and neovascularization. Circumstantial evidence also links PVAT to the pathogenesis of aortic aneurysms and vasculitic syndromes, such as Takayasu's arteritis, where infiltration and migration of inflammatory cells from PVAT into the vascular wall may play a contributory role. Moreover, in obesity, PVAT has been implicated to promote stiffness of elastic arteries via the production of reactive oxygen species. This review will discuss the growing body of data and mechanisms linking PVAT to the pathogenesis of non-atherosclerotic vascular diseases in experimental animal models and in humans.
Highlights
KEY CONCEPTSAccumulating data suggest that PVAT plays an important role in atherosclerosis and hypertension, and in non-atherosclerotic vascular diseases
Perivascular (PV) adipose tissue (PVAT) surrounds most large blood vessels except the cerebral vasculature, juxtaposed to the vascular adventitia and devoid of an anatomical barrier
A growing body of data support linkages between PVAT and non-atherosclerotic vascular diseases, including neointimal hyperplasia, aortic aneurysm, arterial stiffness, and vasculitic syndromes, in experimental animal models and in humans. These diseases are all associated with vascular wall inflammation that may be modulated by adipocytokines produced by PVAT
Summary
Accumulating data suggest that PVAT plays an important role in atherosclerosis and hypertension, and in non-atherosclerotic vascular diseases. Phenotypic changes in PVAT after vascular injury promote release of adipocytokines that can regulate inflammation, VSMC proliferation and neovascularization, thereby contributing to neointimal formation. Phenotypic changes in PVAT in response to high fat diet or smoking may promote vascular inflammation, ROS production, VSMC phenotype switching and matrix degradation to augment AAA formation. Inflamed PVAT is associated with arterial stiffness and vasculitis; direct evidence of a pathologic role of PVAT is lacking. Much of the available data linking PVAT to non-atherosclerotic vascular diseases is associative rather than direct in nature due to the challenges in developing specific experimental models to test the impact of PVAT on these disease states
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