Regional differences in perivascular adipose tissue impacting vascular homeostasis

Gil‐Ortega, Marta; Somoza, Beatriz; Huang, Yü; Gollasch, Maik; Fernández-Alfonso, Marı́a S.

doi:10.1016/j.tem.2015.04.003

Cited by 117 publications

(114 citation statements)

References 78 publications

(130 reference statements)

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“…PVAT surrounds large arteries and veins, small and resistance vessels, and skeletal muscle microvessels. Other microvasculatures and the cerebral vasculature are free of PVAT (Brown et al, ; Gil‐Ortega et al, ). In contrast to humans and other large experimental animals (including rabbits and pigs), the murine coronary artery is without PVAT (Brown et al, ).…”

Section: Pvat: General Aspectsmentioning

confidence: 99%

“…Large vessels (such as the saphenous vein) are separated from PVAT by an anatomical barrier that is rich in collagen bundles, elastin networks, VSMCs, fibroblasts, autonomic nerve endings and vasa vasorum (Ahmed et al, ). In small vessels and microvessels, however, PVAT is an integral part of the vascular wall without laminar structures or any organized barrier separating PVAT from the adventitia (Szasz and Webb, ; Gil‐Ortega et al, ).…”

Section: Pvat: General Aspectsmentioning

confidence: 99%

“…It is proposed that factors released by the PVAT reach the medial and endothelial layer of blood vessels either by direct diffusion or via the vasa vasorum (Gil‐Ortega et al, ). Another possible way for PVAT‐derived factors to reach the inner layers of the vascular wall is via the small media conduits, a dense reticular network of collagenous conduits connecting the medial layer with the underlying adventitia (Grabner et al, ; Campbell et al, ).…”

Section: Pvat: General Aspectsmentioning

confidence: 99%

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The role of perivascular adipose tissue in obesity‐induced vascular dysfunction

Xia

2016

British J Pharmacology

159

152

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Under physiological conditions, perivascular adipose tissue (PVAT) attenuates agonist‐induced vasoconstriction by releasing vasoactive molecules including hydrogen peroxide, angiotensin 1–7, adiponectin, methyl palmitate, hydrogen sulfide, NO and leptin. This anticontractile effect of PVAT is lost under conditions of obesity. The central mechanism underlying this PVAT dysfunction in obesity is likely to be an ‘obesity triad’ (consisting of PVAT hypoxia, inflammation and oxidative stress) that leads to the impairment of PVAT‐derived vasoregulators. The production of hydrogen sulfide, NO and adiponectin by PVAT is reduced in obesity, whereas the vasodilator response to leptin is impaired (vascular leptin resistance). Strikingly, the vasodilator response to acetylcholine is reduced only in PVAT‐containing, but not in PVAT‐free thoracic aorta isolated from diet‐induced obese mice, indicating a unique role for PVAT in obesity‐induced vascular dysfunction. Furthermore, PVAT dysfunction has also been observed in small arteries isolated from the gluteal/visceral fat biopsy samples of obese individuals. Therefore, PVAT may represent a new therapeutic target for vascular complications in obesity. A number of approaches are currently being tested under experimental conditions. Potential therapeutic strategies improving PVAT function include body weight reduction, enhancing PVAT hydrogen sulfide release (e.g. rosiglitazone, atorvastatin and cannabinoid CB1 receptor agonists) and NO production (e.g. arginase inhibitors), inhibition of the renin–angiotensin–aldosterone system, inhibition of inflammation with melatonin or cytokine antagonists, activators of AMP‐activated kinase (e.g. metformin, resveratrol and diosgenin) and adiponectin releasers or expression enhancers.Linked ArticlesThis article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue – Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc

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Section: Pvat: General Aspectsmentioning

confidence: 99%

Section: Pvat: General Aspectsmentioning

confidence: 99%

Section: Pvat: General Aspectsmentioning

confidence: 99%

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The role of perivascular adipose tissue in obesity‐induced vascular dysfunction

Xia

2016

British J Pharmacology

159

152

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“…In mouse models, increased C3 and C4 deposition have been found connected to the adventitial and medial fibers including collagen and elastin at early time points prior to luminal lesion development (8). The detection of C3 and C4 depositions on the outside layers of the vasculature, which are usually surrounded by a local fat depot known as perivascular fat (11), suggested this fat depot as a potential local source of these proteins. Interestingly, postmenopausal women have higher volumes of cardiovascular fat (3).…”

Section: Introductionmentioning

confidence: 99%

Complement proteins and arterial calcification in middle aged women: Cross-sectional effect of cardiovascular fat. The SWAN Cardiovascular Fat Ancillary Study

et al. 2015

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Background CVD risk increases in women after menopause. Recent data suggest higher levels of complement protein C3 and cardiovascular fat (CF) in postmenopausal women. Whether complement proteins are associated with early markers of atherosclerosis in healthy midlife women has never been evaluated. Additionally, the potential impact of the local CF on these associations has never been assessed. Methods Participants (n=100, age (mean(SD)):50.48(2.63), 50% premenopausal) were from the Study of Women's Health Across the Nation (SWAN). Arterial calcification (aortic-AC and coronary-CAC) and CF volumes around the heart and aorta (total heart-TAT and aortic perivascular adipose tissue-PVAT) were quantified using EBCT scans. AC and CAC were each evaluated as presence (Agatston scores>0) and extent of calcification (log (Agatston scores +1)). Logistic and linear regression models were used for statistical analysis. Results Adjusting for age, race, menopausal status and lipids, C3 was significantly associated with both presence and extent of AC and CAC, all P values <0.05. Associations between C3 and presence and extent of AC and CAC were explained by additional adjustment for logTAT and logPVAT, respectively. Association between C3 and log(AC+1) was more pronounced at higher volumes of logTAT (interaction-P=0.013) adjusting for study variables. No associations were found with C4. Conclusions Higher C3 was significantly associated with presence and greater extent of arterial calcification in midlife women. These associations were explained by higher volumes of CF, suggesting CF as a potential source of C3. C3 could be a potential non-invasive biomarker of early diagnosis of atherosclerosis. These findings need to be replicated in larger studies.

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“…Indeed, adipose tissue is an endocrine organ and releases various biological activities including adipokines [37]. PVAT produces some protective substances such as adiponectin, which helps maintain normal physiological arterial function [38, 39]. However, in individuals with obesity and insulin resistance there is increased release of pro-inflammatory adipokines including interleukin-6, interleukin-8, tumor necrosis factor alpha, as well as toll-like receptor-4 [18].…”

Section: Pathological Mechanisms Of Excessive Arterial Stiffnessmentioning

confidence: 99%

Potential Role of Antihypertensive Medications in Preventing Excessive Arterial Stiffening

et al. 2018

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The Framingham Heart Study demonstrated that arterial stiffness is an independent predictor of CVD and related morbidity and mortality. Dysfunction of endothelial cells, vascular smooth muscle cells, extracellular matrix, and other functional elements of the vessel wall contribute to underlying pathophysiology of increased arterial stiffness. An activated renin-angiotensin-aldosterone system, oxidative stress, abnormal peri-vascular adipose tissue, inflammation, and increased sympathetic nervous system activity are associated with the development and progression of arterial fibrosis, stiffening, and associated CVD. In this review, we will discuss the structural and function changes and mechanisms of the vessel wall in arterial stiffness and provide potential therapeutic strategies.

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Regional differences in perivascular adipose tissue impacting vascular homeostasis

Cited by 117 publications

References 78 publications

The role of perivascular adipose tissue in obesity‐induced vascular dysfunction

The role of perivascular adipose tissue in obesity‐induced vascular dysfunction

Complement proteins and arterial calcification in middle aged women: Cross-sectional effect of cardiovascular fat. The SWAN Cardiovascular Fat Ancillary Study

Potential Role of Antihypertensive Medications in Preventing Excessive Arterial Stiffening

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