Abstract
Initially thought to only provide mechanical support for the underlying blood vessels, perivascular adipose tissue (PVAT) has now emerged as a regulator of vascular function. A healthy PVAT exerts anticontractile and anti-inflammatory actions on the underlying vasculature via the release of adipocytokines such as adiponectin, nitric oxide, and omentin. However, dysfunctional PVAT produces more proinflammatory adipocytokines such as leptin, resistin, interleukin- (IL-) 6, IL-1β, and tumor necrosis factor-alpha, thus inducing an inflammatory response that contributes to the pathogenesis of vascular diseases. In this review, current knowledge on the role of PVAT inflammation in the development of vascular pathologies such as atherosclerosis and hypertension was discussed.
Highlights
Cardiovascular diseases (CVD) have been widely known for decades as the leading cause of mortality worldwide
Perivascular adipose tissue (PVAT) surrounds most blood vessels and has been implicated in the pathophysiology of CVD due to its proximity and crosstalk with the underlying vasculature, with PVAT inflammation suggested to be contributing to the development of vascular diseases
PVAT inflammation plays a mechanistic role in the pathogenesis of vascular diseases such as atherosclerosis and hypertension (Table 2)
Summary
Cardiovascular diseases (CVD) have been widely known for decades as the leading cause of mortality worldwide. According to the World Health Organization (WHO), in 2019, an estimated 17.9 million deaths due to CVD were recorded, representing 32% of global deaths [1]. A link between PVAT, inflammation, and CVD was first discovered two decades ago when a study showed an increase in leukocyte infiltration in the PVAT in response to coronary angioplasty [2]. This signifies the role of PVAT inflammation in the pathophysiology of CVD and as a potential future therapeutic target
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