Perivascular adipose tissue and vascular disease

Britton, Kathryn; Fox, Caroline S.

doi:10.2217/clp.10.89

Cited by 110 publications

(80 citation statements)

References 85 publications

(119 reference statements)

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“…Development of insulin resistance has classically been attributed to adipocyte-derived inflammation, resulting in macrophage infiltration and altered secretory profile of adipose tissue depots with increased levels of pro-inflammatory cytokines and decreased Ad synthesis and release [84][85][86]. The differential role of regional fat depots in synthesis and release of specific mediators and vasoactive substances may help to reconcile the generally accepted 'outside-in' theory of vascular inflammation, which postulates that inflammation begins in adipose tissue and then spreads inward to the vasculature [87], with the 'inside-out' process of vascular inflammation, proposing that the first step is intimal injury, that then extends to the media and adventitia [88,89]. For example, it is plausible that intimate connections between perivascular adipose tissue (PVAT) and other components of the vessel wall result in PVAT being the first adipose depot to sense and respond to signals from circulating bioactive factors that influence activity of endothelial and vascular smooth muscle cells [90][91][92].…”

Section: Endothelial Dysfunction and Metaflammationmentioning

confidence: 99%

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Potenza

Nacci

Salvia

et al. 2017

Pharmacological Research

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Abstract:The association of obesity and diabetes, termed "diabesity", defines a combination of primarily metabolic disorders with insulin resistance as the underlying common pathophysiology. Cardiovascular disorders associated with diabesity represent the leading cause of morbidity and mortality in the Western world. This makes diabesity, with its rising impacts on both health and economics, one of the most challenging biomedical and social threats of present century. The emerging comprehension of the genes whose alteration confers inter-individual differences on risk factors for diabetes or obesity, together with the potential role of genetically determined variants on mechanisms controlling responsiveness, effectiveness and safety of anti-diabetic therapy underlines the need of additional knowledge on molecular mechanisms involved in the pathophysiology of diabesity. Endothelial cell dysfunction, resulting from the unbalanced production of endothelialderived vascular mediators, is known to be present at the earliest stages of insulin resistance and obesity, and may precede the clinical diagnosis of diabetes by several years. Once considered as a mere consequence of metabolic abnormalities, it is now clear that endothelial dysfunctional activity may play a pivotal role in the progression of diabesity. In the vicious circle where vascular defects and metabolic disturbances worsen and reinforce each other, a low-grade, chronic, and 'cold' inflammation (metaflammation) has been suggested to serve as the pathophysiological link that binds endothelial and metabolic dysfunctions. In this paradigm, it is important to consider how traditional antidiabetic treatments (specifically addressing metabolic dysregulation) may directly impact on inflammatory processes or cardiovascular function. Indeed, not all drugs currently available to treat diabetes possess the same anti-inflammatory potential, or target endothelial cell function equally. Perspective strategies pointing at reducing metaflammation or directly addressing endothelial dysfunction may disclose beneficial consequences on metabolic regulation. This review focuses on existing and potential new approaches ameliorating endothelial dysfunction and vascular inflammation in the context of diabesity.

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Section: Endothelial Dysfunction and Metaflammationmentioning

confidence: 99%

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Potenza

Nacci

Salvia

et al. 2017

Pharmacological Research

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“…Given its anatomical proximity to the vascular wall, perivascular AT (PVAT) has been identified as a key player in both cardiovascular homeostasis and disease 4. Contrary to distant AT depots that regulate cardiovascular biology by contributing to a circulating pool of bioactive adipocytokines, PVAT is able to directly modulate key signalling pathways in the vascular wall and myocardium through paracrine and vasocrine routes 5.…”

Section: Introductionmentioning

confidence: 99%

“…This includes periaortic fat, as well as organ-specific fat depots located close to major vessels, including the epicardial, pericardial and perirenal AT depots 4. As with any AT depot, PVAT is composed of various cell types such as adipocytes, preadipocytes and mesenchymal stem cells, embedded in a matrix that is invested in microvessels 4.…”

Section: Introductionmentioning

confidence: 99%

Perivascular adipose tissue and coronary atherosclerosis

Mâncio

Oikonomou

Antoniades

2018

Heart

105

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Adipose tissue (AT) is no longer viewed as a passive, energy-storing depot, and a growing body of evidence supports the concept that both quantitative and qualitative aspects of AT are critical in determining an individual's cardiometabolic risk profile. Among all AT sites, perivascular AT (PVAT) has emerged as a depot with a distinctive biological significance in cardiovascular disease given its close anatomical proximity to the vasculature. Recent studies have suggested the presence of complex, bidirectional paracrine and vasocrine signalling pathways between the vascular wall and its PVAT, with far-reaching implications in cardiovascular diagnostics and therapeutics. In this review, we first discuss the biological role of PVAT in both cardiovascular health and disease, highlighting its dual pro-atherogenic and anti-atherogenic roles, as well as potential therapeutic targets in cardiovascular disease. We then review current evidence and promising new modalities on the non-invasive imaging of epicardial AT and PVAT. Specifically, we present how our expanding knowledge on the bidirectional interplay between the vascular wall and its PVAT can be translated into novel clinical diagnostics tools to assess coronary inflammation. To this end, we present the example of a new CT-based method that tracks spatial changes in PVAT phenotype to extract information about the inflammatory status of the adjacent vasculature, highlighting the numerous diagnostic and therapeutic opportunities that arise from our increased understanding of PVAT biology.

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“…Perivascular adipose tissue (PVAT), a local deposit of adipose tissue surrounding the vasculature, is present throughout the body [2], and has been shown to have a local regulation effect on blood vessels. While its components are heterogeneous, the PVAT is mainly composed of adipocytes.…”

mentioning

confidence: 99%

Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone acetate‐salt hypertensive mice

Lijuan

Ruan

et al. 2016

FEBS Letters

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Edited by Laszlo NagyBeta3 adrenergic receptor (ADRB3) mediates vessel relaxation in the endothelium while it modulates lipolysis in the adipose tissue. However, the function and regulation mechanism of ADRB3 in the perivascular adipose tissue (PVAT), especially in hypertension, is still unclear. We show that ADRB3 protein is upregulated in the PVAT of deoxycorticosterone acetatesalt (DOCA-salt) hypertensive mice, with the characteristics of PVAT browning and increased uncoupling protein 1 (UCP1) expression. Inhibition of ADRB3 with selective antagonist SR59230A caused serious vascular injury in vivo, even though UCP1 expression was downregulated. ADRB3 protein was regulated by let-7b, which was decreased in the PVAT of the DOCA-salt group. These data reveal that ADRB3 in PVAT contributes to vascular function in the progression of hypertension.

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Perivascular adipose tissue and vascular disease

Cited by 110 publications

References 85 publications

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options

Perivascular adipose tissue and coronary atherosclerosis

Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone acetate‐salt hypertensive mice

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