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    The role of perivascular adipose tissue in obesity-induced vascular dysfunction. Xia Ning,Li Huige British journal of pharmacology 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 CB 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 ARTICLES:This 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. 10.1111/bph.13650
    Remote Effects of Transplanted Perivascular Adipose Tissue on Endothelial Function and Atherosclerosis. Horimatsu Tetsuo,Patel Aaron S,Prasad Rosaria,Reid Lauren E,Benson Tyler W,Zarzour Abdalrahman,Ogbi Mourad,Bruder do Nascimento Thiago,Belin de Chantemele Eric,Stansfield Brian K,Lu Xin-Yun,Kim Ha Won,Weintraub Neal L Cardiovascular drugs and therapy PURPOSE:Perivascular adipose tissue (PVAT) surrounds the arterial adventitia and plays an important role in vascular homeostasis. PVAT expands in obesity, and inflamed PVAT can locally promote endothelial dysfunction and atherosclerosis. Here, using adipose tissue transplantation, we tested the hypothesis that expansion of PVAT can also remotely exacerbate vascular disease. METHODS:Fifty milligrams of abdominal aortic PVAT was isolated from high-fat diet (HFD)-fed wild-type mice and transplanted onto the abdominal aorta of lean LDL receptor knockout mice. Subcutaneous and visceral adipose tissues were used as controls. After HFD feeding for 10 weeks, body weight, glucose/insulin sensitivity, and lipid levels were measured. Adipocytokine gene expression was assessed in the transplanted adipose tissues, and the thoracic aorta was harvested to quantify atherosclerotic lesions by Oil-Red O staining and to assess vasorelaxation by wire myography. RESULTS:PVAT transplantation did not influence body weight, fat composition, lipid levels, or glucose/insulin sensitivity. However, as compared with controls, transplantation of PVAT onto the abdominal aorta increased thoracic aortic atherosclerosis. Furthermore, PVAT transplantation onto the abdominal aorta inhibited endothelium-dependent relaxation in the thoracic aorta. MCP-1 and TNF-α expression was elevated, while adiponectin expression was reduced, in the transplanted PVAT tissue, suggesting augmented inflammation as a potential mechanism for the remote vascular effects of transplanted PVAT. CONCLUSIONS:These data suggest that PVAT expansion and inflammation in obesity can remotely induce endothelial dysfunction and augment atherosclerosis. Identifying the underlying mechanisms may lead to novel approaches for risk assessment and treatment of obesity-related vascular disease. 10.1007/s10557-018-6821-y
    Exploring the Relationship of Perivascular Adipose Tissue Inflammation and the Development of Vascular Pathologies. Rami Afifah Zahirah Abd,Hamid Adila A,Anuar Nur Najmi Mohamad,Aminuddin Amilia,Ugusman Azizah Mediators of inflammation 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-1, 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. 10.1155/2022/2734321
    Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling. Nature communications Although inflammation plays critical roles in the development of atherosclerosis, its regulatory mechanisms remain incompletely understood. Perivascular adipose tissue (PVAT) has been reported to undergo inflammatory changes in response to vascular injury. Here, we show that vascular injury induces the beiging (brown adipose tissue-like phenotype change) of PVAT, which fine-tunes inflammatory response and thus vascular remodeling as a protective mechanism. In a mouse model of endovascular injury, macrophages accumulate in PVAT, causing beiging phenotype change. Inhibition of PVAT beiging by genetically silencing PRDM16, a key regulator to beiging, exacerbates inflammation and vascular remodeling following injury. Conversely, activation of PVAT beiging attenuates inflammation and pathological vascular remodeling. Single-cell RNA sequencing reveals that beige adipocytes abundantly express neuregulin 4 (Nrg4) which critically regulate alternative macrophage activation. Importantly, significant beiging is observed in the diseased aortic PVAT in patients with acute aortic dissection. Taken together, vascular injury induces the beiging of adjacent PVAT with macrophage accumulation, where NRG4 secreted from the beige PVAT facilitates alternative activation of macrophages, leading to the resolution of vascular inflammation. Our study demonstrates the pivotal roles of PVAT in vascular inflammation and remodeling and will open a new avenue for treating atherosclerosis. 10.1038/s41467-022-32658-6
    Potential role of perivascular adipose tissue in modulating atherosclerosis. Ahmadieh Samah,Kim Ha Won,Weintraub Neal L Clinical science (London, England : 1979) Perivascular adipose tissue (PVAT) directly juxtaposes the vascular adventitia and contains a distinct mixture of mature adipocytes, preadipocytes, stem cells, and inflammatory cells that communicate via adipocytokines and other signaling mediators with the nearby vessel wall to regulate vascular function. Cross-talk between perivascular adipocytes and the cells in the blood vessel wall is vital for normal vascular function and becomes perturbed in diseases such as atherosclerosis. Perivascular adipocytes surrounding coronary arteries may be primed to promote inflammation and angiogenesis, and PVAT phenotypic changes occurring in the setting of obesity, hyperlipidemia etc., are fundamentally important in determining a pathogenic versus protective role of PVAT in vascular disease. Recent discoveries have advanced our understanding of the role of perivascular adipocytes in modulating vascular function. However, their impact on cardiovascular disease (CVD), particularly in humans, is yet to be fully elucidated. This review will highlight the complex mechanisms whereby PVAT regulates atherosclerosis, with an emphasis on clinical implications of PVAT and emerging strategies for evaluation and treatment of CVD based on PVAT biology. 10.1042/CS20190577
    Perivascular Adipose Tissue and Vascular Perturbation/Atherosclerosis. Kim Ha Won,Shi Hong,Winkler Michael A,Lee Richard,Weintraub Neal L Arteriosclerosis, thrombosis, and vascular biology Atherosclerosis is orchestrated by complex interactions between vascular and inflammatory cells. Traditionally, it has been considered to be an intimal inflammatory disease, characterized by endothelial dysfunction, inflammatory cell recruitment, lipid oxidation, and foam cell formation. This inside-out signaling paradigm has been accepted as dogma for many years, despite the fact that inflammatory cells are far more prevalent in the adventitia compared with the intima. For decades, the origin of adventitial inflammation in atherosclerosis was unknown. The fact that these inflammatory cells were observed to cluster at the margin of perivascular adipose tissues-a unique and highly inflammatory adipose depot that surrounds most atherosclerosis-prone blood vessels-has stimulated interest in perivascular adipose tissue-mediated outside-in signaling in vascular pathophysiology, including atherosclerosis. The phenotype of perivascular adipocytes underlies the functional characteristics of this depot, including its role in adventitial inflammatory cell recruitment, trafficking to the intima via the vasa vasorum, and atherosclerosis perturbation. This review is focused on emerging concepts pertaining to outside-in signaling in atherosclerosis driven by dysfunctional perivascular adipose tissues during diet-induced obesity and recent strategies for atherosclerosis prediction and prognostication based upon this hypothesis. 10.1161/ATVBAHA.120.312470
    Emerging Roles of Sympathetic Nerves and Inflammation in Perivascular Adipose Tissue. Cardiovascular drugs and therapy Perivascular adipose tissue (PVAT) is no longer recognised as simply a structural support for the vasculature, and we now know that PVAT releases vasoactive factors which modulate vascular function. Since the discovery of this function in 1991, PVAT research is rapidly growing and the importance of PVAT function in disease is becoming increasingly clear. Obesity is associated with a plethora of vascular conditions; therefore, the study of adipocytes and their effects on the vasculature is vital. PVAT contains an adrenergic system including nerves, adrenoceptors and transporters. In obesity, the autonomic nervous system is dysfunctional; therefore, sympathetic innervation of PVAT may be the key mechanistic link between increased adiposity and vascular disease. In addition, not all obese people develop vascular disease, but a common feature amongst those that do appears to be the inflammatory cell population in PVAT. This review will discuss what is known about sympathetic innervation of PVAT, and the links between nerve activation and inflammation in obesity. In addition, we will examine the therapeutic potential of exercise in sympathetic stimulation of adipose tissue. 10.1007/s10557-019-06862-4
    The Role of Perivascular Adipose Tissue in Non-atherosclerotic Vascular Disease. Horimatsu Tetsuo,Kim Ha Won,Weintraub Neal L Frontiers in physiology 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. 10.3389/fphys.2017.00969
    Perivascular Adipose Tissue Inflammation in Ischemic Heart Disease. Mazzotta Celestina,Basu Sanchita,Gower Adam C,Karki Shakun,Farb Melissa G,Sroczynski Emily,Zizza Elaina,Sarhan Anas,Pande Ashvin N,Walsh Kenneth,Dobrilovic Nikola,Gokce Noyan Arteriosclerosis, thrombosis, and vascular biology OBJECTIVE:There is growing recognition that adipose tissue-derived proatherogenic mediators contribute to obesity-related cardiovascular disease. We sought to characterize regional differences in perivascular adipose tissue (PVAT) phenotype in relation to atherosclerosis susceptibility. Approach and Results: We examined thoracic PVAT samples in 34 subjects (body mass index 32±6 kg/m, age 59±11 years) undergoing valvular, aortic, or coronary artery bypass graft surgeries and performed transcriptomic characterization using whole-genome expression profiling and quantitative polymerase chain reaction analyses. We identified a highly inflamed region of PVAT surrounding the human aortic root in close proximity to coronary takeoff and adjoining epicardial fat. In subjects undergoing coronary artery bypass graft, we found 300 genes significantly upregulated (false discovery rate <0.1) in paired samples of PVAT surrounding the aortic root compared with nonatherosclerotic left internal mammary artery. Genes encoding proteins mechanistically implicated in atherogenesis were enriched in aortic PVAT consisting of signaling pathways linked to inflammation, (wingless-related integration site) signaling, matrix remodeling, coagulation, and angiogenesis. Overexpression of several proatherogenic transcripts, including , (), and , were confirmed by quantitative polymerase chain reaction and significantly bolstered in coronary artery disease subjects. Angiographic coronary artery disease burden quantified by the Gensini score positively correlated with the expression of inflammatory genes in PVAT. Moreover, periaortic adipose inflammation was markedly higher in obese subjects with striking upregulation (≈8-fold) of expression compared to nonobese individuals. CONCLUSIONS:Proatherogenic mediators that originate from dysfunctional PVAT may contribute to vascular disease mechanisms in human vessels. Moreover, PVAT may adopt detrimental properties under obese conditions that play a key role in the pathophysiology of ischemic heart disease. Graphic Abstract: A graphic abstract is available for this article. 10.1161/ATVBAHA.120.315865
    Obesity, Adipose Tissue and Vascular Dysfunction. Koenen Mascha,Hill Michael A,Cohen Paul,Sowers James R Circulation research Cardiovascular diseases are the leading cause of death worldwide. Overweight and obesity are strongly associated with comorbidities such as hypertension and insulin resistance, which collectively contribute to the development of cardiovascular diseases and resultant morbidity and mortality. Forty-two percent of adults in the United States are obese, and a total of 1.9 billion adults worldwide are overweight or obese. These alarming numbers, which continue to climb, represent a major health and economic burden. Adipose tissue is a highly dynamic organ that can be classified based on the cellular composition of different depots and their distinct anatomical localization. Massive expansion and remodeling of adipose tissue during obesity differentially affects specific adipose tissue depots and significantly contributes to vascular dysfunction and cardiovascular diseases. Visceral adipose tissue accumulation results in increased immune cell infiltration and secretion of vasoconstrictor mediators, whereas expansion of subcutaneous adipose tissue is less harmful. Therefore, fat distribution more than overall body weight is a key determinant of the risk for cardiovascular diseases. Thermogenic brown and beige adipose tissue, in contrast to white adipose tissue, is associated with beneficial effects on the vasculature. The relationship between the type of adipose tissue and its influence on vascular function becomes particularly evident in the context of the heterogenous phenotype of perivascular adipose tissue that is strongly location dependent. In this review, we address the abnormal remodeling of specific adipose tissue depots during obesity and how this critically contributes to the development of hypertension, endothelial dysfunction, and vascular stiffness. We also discuss the local and systemic roles of adipose tissue derived secreted factors and increased systemic inflammation during obesity and highlight their detrimental impact on cardiovascular health. 10.1161/CIRCRESAHA.121.318093
    Perivascular adipose tissue inflammation in vascular disease. Nosalski Ryszard,Guzik Tomasz J British journal of pharmacology Perivascular adipose tissue (PVAT) plays a critical role in the pathogenesis of cardiovascular disease. In vascular pathologies, perivascular adipose tissue increases in volume and becomes dysfunctional, with altered cellular composition and molecular characteristics. PVAT dysfunction is characterized by its inflammatory character, oxidative stress, diminished production of vaso-protective adipocyte-derived relaxing factors and increased production of paracrine factors such as resistin, leptin, cytokines (IL-6 and TNF-α) and chemokines [RANTES (CCL5) and MCP-1 (CCL2)]. These adipocyte-derived factors initiate and orchestrate inflammatory cell infiltration including primarily T cells, macrophages, dendritic cells, B cells and NK cells. Protective factors such as adiponectin can reduce NADPH oxidase superoxide production and increase NO bioavailability in the vessel wall, while inflammation (e.g. IFN-γ or IL-17) induces vascular oxidases and eNOS dysfunction in the endothelium, vascular smooth muscle cells and adventitial fibroblasts. All of these events link the dysfunctional perivascular fat to vascular dysfunction. These mechanisms are important in the context of a number of cardiovascular disorders including atherosclerosis, hypertension, diabetes and obesity. Inflammatory changes in PVAT's molecular and cellular responses are uniquely different from classical visceral or subcutaneous adipose tissue or from adventitia, emphasizing the unique structural and functional features of this adipose tissue compartment. Therefore, it is essential to develop techniques for monitoring the characteristics of PVAT and assessing its inflammation. This will lead to a better understanding of the early stages of vascular pathologies and the development of new therapeutic strategies focusing on perivascular adipose tissue. LINKED ARTICLES:This 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. 10.1111/bph.13705
    Role of Inflammation in Vascular Disease-Related Perivascular Adipose Tissue Dysfunction. Chen Yaozhi,Qin Zeyu,Wang Yaqiong,Li Xin,Zheng Yang,Liu Yunxia Frontiers in endocrinology Perivascular adipose tissue (PVAT) is the connective tissue around most blood vessels throughout the body. It provides mechanical support and maintains vascular homeostasis in a paracrine/endocrine manner. Under physiological conditions, PVAT has anti-inflammatory effects, improves free fatty acid metabolism, and regulates vasodilation. In pathological conditions, PVAT is dysfunctional, secretes many anti-vasodilator factors, and participates in vascular inflammation through various cells and mediators; thus, it causes dysfunction involving vascular smooth muscle cells and endothelial cells. Inflammation is an important pathophysiological event in many vascular diseases, such as vascular aging, atherosclerosis, and hypertension. Therefore, the pro-inflammatory crosstalk between PVAT and blood vessels may comprise a novel therapeutic target for the prevention and treatment of vascular diseases. In this review, we summarize findings concerning PVAT function and inflammation in different pathophysiological backgrounds, focusing on the secretory functions of PVAT and the crosstalk between PVAT and vascular inflammation in terms of vascular aging, atherosclerosis, hypertension, diabetes mellitus, and other diseases. We also discuss anti-inflammatory treatment for potential vascular diseases involving PVAT. 10.3389/fendo.2021.710842
    Perivascular fat attenuation index and high-risk plaque features evaluated by coronary CT angiography: relationship with serum inflammatory marker level. Dai Xu,Deng Jianhong,Yu Mengmeng,Lu Zhigang,Shen Chengxing,Zhang Jiayin The international journal of cardiovascular imaging The present study aimed to investigate the association between perivascular fat attenuation index (FAI), high-risk plaque features and serum level of high sensitive C-reactive protein (hs-CRP). Consecutive patients with intermediate pre-test probability of CAD, who were referred for coronary CT angiography (CCTA), were included. High-risk plaque features were assessed by CCTA and included low attenuation plaque (LAP), positive remodeling (PR), napkin-ring sign (NRS) and spotty calcification. Lesion specific perivascular FAI was also measured for all plaques located on major epicardial vessels with diameter ≧ 2 mm. Laboratory test results, including hs-CRP, were recorded. 199 patients with 260 lesions were finally included. NRS and LAP were more commonly present in the group with elevated hs-CRP (35.9% vs. 19.4% and 14.1% vs. 2.6%, both p < 0.05) and more severe stenosis extent was also noted for this group. However, there was no significant difference between the elevated hs-CRP and normal hs-CRP group with respect to other CT parameters, such as lesion length, PR, spotty calcification and focal calcium score. Perivascular FAI failed to show significant difference between the two groups (- 69.8 ± 10.3HU vs. - 70.0 ± 12.0HU, p = 0.953) and there was poor correlation between perivascular FAI and hs-CRP measurements (r =  - 0.04, p = 0.510). In conclusion, LAP and NRS are more commonly present in CAD patients with elevated level of hs-CRP. However, perivascular FAI failed to show such correlation with serum level of hs-CRP. 10.1007/s10554-019-01758-8
    Serial change of perivascular fat attenuation index after statin treatment: Insights from a coronary CT angiography follow-up study. Dai Xu,Yu Lihua,Lu Zhigang,Shen Chengxing,Tao Xinwei,Zhang Jiayin International journal of cardiology BACKGROUND:Perivascular fat attenuation index (FAI) was thought to be an indicator of active vessel inflammation surrounding coronary plaques. However, whether this index can be reduced by statin treatment remains unknown. We aimed to investigate the serial change of lesion-specific perivascular FAI as quantified by coronary computed tomography (CCTA) after statin treatment. METHODS:Consecutive patients with chest pain and intermediate likelihood of coronary artery disease were referred for baseline CCTA. Patients were retrospectively included if they were treated medically and underwent follow-up CCTA at 1-year to 1.5-year interval. Lesion-specific perivascular FAI, as well as other plaque features, were measured at baseline and follow-up. RESULTS:One hundred and eight patients (mean age 67.7 ± 11.1, 76 males) were included. A significant reduction of the FAI value was found for non-calcified plaques and mixed plaques (-68.0 HU ± 8.5 HU Vs. -71.5 HU ± 8.1 HU, p < .001 and - 70.5 HU ± 8.9 HU Vs. -72.8 HU ± 9.0 HU, p = .014). However, this improvement was not observed for calcified plaques (-70.6 HU ± 9.7 HU Vs. -71.7 HU ± 9.9 HU, p = .258). For non-calcified and mixed plaques, the volumes of non-calcified as well as low attenuation component was significantly reduced whereas total plaque volume and volume of calcified component increased. For calcified plaque, total plaque volume also demonstrated remarkable increase after statin treatment CONCLUSIONS: Lesion-specific perivascular FAI decreased at mid-term follow-up after statin treatment for non-calcified and mixed plaques. Perivascular FAI can be a potential imaging biomarker to monitor the anti-inflammation response to statin treatments. 10.1016/j.ijcard.2020.06.008
    Perivascular adipose tissue in age-related vascular disease. Queiroz Marcelo,Sena Cristina M Ageing research reviews Perivascular adipose tissue (PVAT), a crucial regulator of vascular homeostasis, is actively involved in vascular dysfunction during aging. PVAT releases various adipocytokines, chemokines and growth factors. In an endocrine and paracrine manner PVAT-derived factors regulate vascular signalling and inflammation modulating functions of adjacent layers of the vasculature. Pathophysiological conditions such as obesity, type 2 diabetes, vascular injury and aging can cause PVAT dysfunction, leading to vascular endothelial and smooth muscle cell dysfunctions. We and others have suggested that PVAT is involved in the inflammatory response of the vascular wall in diet induced obesity animal models leading to vascular dysfunction due to disappearance of the physiological anticontractile effect. Previous studies confirm a crucial role for pinpointed PVAT inflammation in promoting vascular oxidative stress and inflammation in aging, enhancing the risk for development of cardiovascular disease. In this review, we discuss several studies and mechanisms linking PVAT to age-related vascular diseases. An overview of the suggested roles played by PVAT in different disorders associated with the vasculature such as endothelial dysfunction, neointimal formation, aneurysm, vascular contractility and stiffness will be performed. PVAT may be considered a potential target for therapeutic intervention in age-related vascular disease. 10.1016/j.arr.2020.101040
    Mechanistic Links Between Obesity, Diabetes, and Blood Pressure: Role of Perivascular Adipose Tissue. Saxton Sophie N,Clark Ben J,Withers Sarah B,Eringa Etto C,Heagerty Anthony M Physiological reviews Obesity is increasingly prevalent and is associated with substantial cardiovascular risk. Adipose tissue distribution and morphology play a key role in determining the degree of adverse effects, and a key factor in the disease process appears to be the inflammatory cell population in adipose tissue. Healthy adipose tissue secretes a number of vasoactive adipokines and anti-inflammatory cytokines, and changes to this secretory profile will contribute to pathogenesis in obesity. In this review, we discuss the links between adipokine dysregulation and the development of hypertension and diabetes and explore the potential for manipulating adipose tissue morphology and its immune cell population to improve cardiovascular health in obesity. 10.1152/physrev.00034.2018
    Imaging residual inflammatory cardiovascular risk. Antoniades Charalambos,Antonopoulos Alexios S,Deanfield John European heart journal Targeting residual cardiovascular risk in primary and secondary prevention, would allow deployment of novel therapeutic agents, facilitating precision medicine. For example, lowering vascular inflammation is a promising strategy to reduce the residual inflammatory cardiovascular risk in patients already receiving optimal medical therapy, but prescribing novel anti-inflammatory treatments will be problematic due to the lack of specific companion diagnostic tests, to guide their targeted use in clinical practice. Currently available tests for the detection of coronary inflammation are either non-specific for the cardiovascular system (e.g. plasma biomarkers) or expensive and not readily available (e.g. hybrid positron emission tomography imaging). Recent technological advancements in coronary computed tomography angiography (CCTA) allow non-invasive detection of high-risk plaque features (positive remodelling, spotty calcification, low attenuation plaque, and napkin-ring sign) and help identify the vulnerable patient, but they provide only indirectly information about coronary inflammation. Perivascular fat attenuation index (FAI), a novel method for assessing coronary inflammation by analysing routine CCTA, captures changes in the perivascular adipose tissue composition driven by inflammatory signals coming from the inflamed coronary artery, by analysing the three-dimensional gradients of perivascular attenuation, followed by adjustments for technical, anatomical, and biological factors. By detecting vascular inflammation, perivascular FAI enhances cardiovascular risk discrimination which could aid more cost-effective deployment of novel therapeutic agents. In this article, we present the existing non-invasive modalities for the detection of coronary inflammation and provide a practical guide for their use in clinical practice. 10.1093/eurheartj/ehz474
    Developmental and functional characteristics of the thoracic aorta perivascular adipocyte. Ye Maoqing,Ruan Cheng-Chao,Fu Mengxia,Xu Lian,Chen Dongrui,Zhu Minsheng,Zhu Dingliang,Gao Pingjin Cellular and molecular life sciences : CMLS Thoracic aorta perivascular adipose tissue (T-PVAT) has critical roles in regulating vascular homeostasis. However, the developmental characteristics and cellular lineage of adipocyte in the T-PVAT remain unclear. We show that T-PVAT contains three long strip-shaped fat depots, anterior T-PVAT (A-T-PVAT), left lateral T-PVAT (LL-T-PVAT), and right lateral T-PVAT (RL-T-PVAT). A-T-PVAT displays a distinct transcriptional profile and developmental origin compared to the two lateral T-PVATs (L-T-PVAT). Lineage tracing studies indicate that A-T-PVAT adipocytes are primarily derived from SM22α progenitors, whereas L-T-PVAT contains both SM22α and Myf5 cells. We also show that L-T-PVAT contains more UCP1 brown adipocytes than A-T-PVAT, and L-T-PVAT exerts a greater relaxing effect on aorta than A-T-PVAT. Angiotensin II-infused hypertensive mice display greater macrophage infiltration into A-T-PVAT than L-T-PVAT. These combined results indicate that L-T-PVAT has a distinct development from A-T-PVAT with different cellular lineage, and suggest that L-T-PVAT and A-T-PVAT have different physiological and pathological functions. 10.1007/s00018-018-2970-1