From the epicardial adipose tissue to vulnerable coronary plaques

Echavarría‐Pinto, Mauro; Hernando, Lorenzo; Alfonso, Fernándo

doi:10.4330/wjc.v5.i4.68

Cited by 10 publications

(10 citation statements)

References 51 publications

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“…Low-density lipoprotein (LDL) cholesterol level and EAT volume were independently associated with the percentage of necrotic plaque tissue. These findings are consistent with previous reports [41] . Moreover, EAT is associated also with microvascular dysfunction in the absence of obstructive CAD.…”

Section: Adipose Tissue Depotssupporting

confidence: 83%

Adipose tissue and vascular inflammation in coronary artery disease

Golia¹,

Limongelli²,

Natale³

et al. 2014

WJC

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Obesity has become an important public health issue in Western and developing countries, with well known metabolic and cardiovascular complications. In the last decades, evidence have been growing about the active role of adipose tissue as an endocrine organ in determining these pathological consequences. As a consequence of the expansion of fat depots, in obese subjects, adipose tissue cells develope a phenotypic modification, which turns into a change of the secretory output. Adipocytokines produced by both adipocytes and adipose stromal cells are involved in the modulation of glucose and lipid handling, vascular biology and, moreover, participate to the systemic inflammatory response, which characterizes obesity and metabolic syndrome. This might represent an important pathophysiological link with atherosclerotic complications and cardiovascular events. A great number of adipocytokines have been described recently, linking inflammatory mileu and vascular pathology. The understanding of these pathways is crucial not only from a pathophysiological point of view, but also to a better cardiovascular disease risk stratification and to the identification of possible therapeutic targets. The aim of this paper is to review the role of Adipocytokines as a possible link between obesity and vascular disease. Key words: Adipocytokines; Obesity; Metabolic syndrome; Coronary artery disease; Inflammation Core tip: Our article, provide a comprehensive review of the evidence about adipose tissue and cardiovascular risk, focusing on the pathophysiological and clinical role of fat-derived mediators, the so-called adipocytokines.

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Section: Adipose Tissue Depotssupporting

confidence: 83%

Adipose tissue and vascular inflammation in coronary artery disease

Golia¹,

Limongelli²,

Natale³

et al. 2014

WJC

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“…Human eAT has also been the focus of significant clinical attention, where using various imaging modalities, multiple studies have indicated that an increase in eAT mass and volume associates with the incidence and occurrence of CAD 1 , 2 , and can even serve as a predictor of future coronary events independent of BMI 6 , 8 , 13 , 34 , 35 . However, a number of such studies do not segregate between eAT and the fat lying outside the pericardium i .…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of the Ucp1-associated oxidative phenotype of human epicardial adipose tissue

Chechi

Voisine

Mathieu

et al. 2017

Sci Rep

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Brown fat presence and metabolic activity has been associated with lower body mass index, higher insulin sensitivity and better cardiometabolic profile in humans. We, and others, have previously reported the presence of Ucp1, a marker of brown adipocytes, in human epicardial adipose tissue (eAT). Characterization of the metabolic activity and associated physiological relevance of Ucp1 within eAT, however, is still awaited. Here, we validate the presence of Ucp1 within human eAT and its ‘beige’ nature. Using in-vitro analytical approaches, we further characterize its thermogenic potential and demonstrate that human eAT is capable of undergoing enhanced uncoupling respiration upon stimulation. Direct biopsy gene expression analysis reveals a negative association between thermogenic markers and oxidative stress-related genes in this depot. Consistently, isoproterenol (Iso) stimulation of eAT leads to a downregulation of secreted proteins included in the GO terms ‘cell redox homeostasis’ and ‘protein folding’. In addition, cardiac endothelial cells exhibit a downregulation in the expression of adhesion markers upon treatment with Iso-stimulated eAT derived conditioned media. Overall, these observations suggest that Ucp1- associated metabolic activity plays a significant role in local tissue homeostasis within eAT and can plausibly alter its communication with neighboring cells of the cardiovascular system.

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“…The plaque rupture arises in the fibrous layer, which is usually thin and heavily infiltrated by macrophages, which are responsible for maintaining a proinflammatory state of the underlying tissue. Furthermore, EAT secretion of TNF- α , IL-1, and MCP-1 stimulates macrophages and induces apoptosis of vascular smooth muscle cells [ 143 , 144 ]; both events might contribute to weakening of the fibrous layer and subsequent cleavage of the plate. However, the precise mechanisms by which the breaking of the plaque occurs have not yet been fully understood [ 144 ].…”

Section: Epicardial Fat In Clinical Practicementioning

confidence: 99%

Epicardial Fat: Physiological, Pathological, and Therapeutic Implications

Salazar

Luzardo

Mejías

et al. 2016

Cardiology Research and Practice

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Epicardial fat is closely related to blood supply vessels, both anatomically and functionally, which is why any change in this adipose tissue's behavior is considered a potential risk factor for cardiovascular disease development. When proinflammatory adipokines are released from the epicardial fat, this can lead to a decrease in insulin sensitivity, low adiponectin production, and an increased proliferation of vascular smooth muscle cells. These adipokines move from one compartment to another by either transcellular passing or diffusion, thus having the ability to regulate cardiac muscle activity, a phenomenon called vasocrine regulation. The participation of these adipokines generates a state of persistent vasoconstriction, increased stiffness, and weakening of the coronary wall, consequently contributing to the formation of atherosclerotic plaques. Therefore, epicardial adipose tissue thickening should be considered a risk factor in the development of cardiovascular disease, a potential therapeutic target for cardiovascular pathology and a molecular point of contact for “endocrine-cardiology.”

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From the epicardial adipose tissue to vulnerable coronary plaques

Cited by 10 publications

References 51 publications

Adipose tissue and vascular inflammation in coronary artery disease

Adipose tissue and vascular inflammation in coronary artery disease

Functional characterization of the Ucp1-associated oxidative phenotype of human epicardial adipose tissue

Epicardial Fat: Physiological, Pathological, and Therapeutic Implications

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