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avoiding formation of hypoxic regions&#44; which are usually associated with inflammation and fibrosis&#46; Differentiation of preadipocytes into mature adipocytes &#40;adipogenesis&#41; occurs along the vascular wall&#44; and angiogenesis is also regulated by adipocyte-derived factors&#44; so that each adipocyte is irrigated by at least one capillary&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">2</span></a> Thus&#44; angiogenesis and adipogenesis are mutually regulated&#44; in what may be called adipovascular coupling&#46; Neovascularization is associated with increased adipocyte number &#40;hyperplasia&#41;&#44; while angiogenesis deficits are associated with larger adipocytes &#40;hypertrophy&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">2</span></a> The adipocyte secretome has been shown to shift from anti-inflammatory&#44; angiogenic and matrix remodeling factors of smaller and irrigated adipocytes&#44; to proinflammatory cytokines&#44; chemokines and profibrotic factors of hypertrophic adipocytes &#40;hepatocyte and fibroblast growth factors&#44; transforming growth factor beta&#44; tumor necrosis factor alpha and matrix metalloproteinases&#41;&#46; These conditions are also associated with an imbalance in angiogenic factors&#44; which leads to alterations in vascular architecture&#44; chronic hypoxia&#44; propagation of the proinflammatory milieu and impairment of other adipokines&#44; such as adiponectin&#44; leptin and resistin&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Epicardial adipose tissue &#40;EAT&#41; is located between the visceral layer of the pericardium and the myocardium&#44; while pericardial adipose tissue is located outside the pericardium&#46; Moreover&#44; EAT is irrigated by the coronary circulation&#44; while pericardial adipose tissue is not&#44; and EAT may also be found around coronary arteries&#44; which may directly influence coronary blood flow&#46; This fat depot is especially rich in preadipocytes&#44; rather than mature adipocytes&#44; and shares some features with brown and beige adipocytes&#44; including UCP1 expression and a higher metabolic rate than other fat pads&#46; EAT has a higher capacity for uptake and release of fatty acids&#44; which is important to sustain myocardial metabolism in physiological conditions&#46; Fatty acid flux is regulated by vasoactive factors released by EAT&#44; which control coronary vessel tone&#46; Besides providing fatty acids for cardiomyocyte metabolism&#44; EAT also protects the myocardium through its mechanical and thermogenic properties&#44; preventing changes in myocardial structure and temperature during contraction&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">EAT is easily detected by common imaging methods such as ultrasonography or computed tomography&#44; which enable its volume to be measured with high accuracy&#46; The relationship between EAT volume and cardiovascular function has been examined in a large number of studies&#46; EAT volume has been correlated with several features of coronary artery disease&#44; including coronary calcification&#44; carotid intima-media thickness and coronary flood flow in patients with coronary artery disease but normal myocardial perfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a> EAT volume was also correlated with poorer left ventricular diastolic function&#44; but not other parameters of ventricular function&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Reduction of EAT volume through physical exercise and sleeve gastrectomy was recently proposed as a promising strategy to reduce atherosclerotic lesions&#44; due to reductions in proinflammatory adipokines and improvement of the inflammatory milieu in the coronary vessel wall&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">6</span></a> Moreover&#44; GLP-1 receptor expression in EAT was recently shown to be linked to genes involved in fatty acid oxidation&#44; and liraglutide was observed to produce a marked decrease in this fat depot&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">7</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The study of EAT is not a simple task because&#44; besides the fact that its collection requires invasive thoracic surgery&#44; it is not found in rodent models&#46; Moreover&#44; EAT is often obtained from chronic patients undergoing surgery&#44; which does not provide information about early metabolic and endocrine alterations of this fat depot&#46; Thus&#44; factors including difficult access&#44; duration of metabolic or cardiac disease and medication may hamper study of the mechanisms linking EAT &#40;dys&#41;function with cardiac disease&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The role of other fat depots was initially reported in the context of the pathophysiology of metabolic syndrome&#44; body mass index &#40;BMI&#41; and adiposity being considered the main risk factors for insulin resistance and glucose intolerance&#46; Nowadays&#44; several years after the first studies&#44; there is a growing body of evidence showing that BMI is not a good predictor of metabolic disease&#44; especially insulin resistance&#46; Instead&#44; various studies have reported that adipose tissue dysfunction&#44; with changes in metabolic and endocrine functions&#44; is more closely associated with insulin resistance-associated diseases&#44; such as type 2 diabetes and non-alcoholic fatty liver disease&#46; Thus&#44; EAT can be expected to undergo various changes in metabolic syndrome&#44; which may be related to its greater proatherogenicity&#46; EAT from type 2 diabetic patients was shown to present infiltration of immune cells &#40;including macrophages&#44; T lymphocytes and dendritic cells&#41; and impaired expression of key genes&#44; with a more proinflammatory profile&#46; This inflammatory infiltration creates a proinflammatory environment that extends to the surrounding vessels and cardiomyocytes&#46; The correlation between EAT volume and changes in systolic and diastolic function was observed to be stronger in type 2 diabetic patients than in controls&#44; suggesting that changes occurring in EAT in type 2 diabetes directly impact myocardial function&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">From an imaging standpoint&#44; good markers of EAT infiltration are necessary&#46; Recently&#44; a study by Liu et al&#46; showed that changes in attenuation&#44; calculated from cardiac computed tomography angiography&#44; are a better predictor of atherosclerosis than EAT volume by itself&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">9</span></a> In molecular terms&#44; impaired EAT secretion of adipokines and profibrotic factors has been observed&#44;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">10</span></a> but little is known regarding the molecular links between EAT &#40;dys&#41;function and cardiovascular function&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Thus&#44; although there is currently some evidence that EAT may be associated with coronary artery disease and other cardiac disease&#44; there is a need for studies able to dissect the molecular links between EAT &#40;dys&#41;function and cardiac disease&#46; In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Mancio et al&#46; describe the protocol of a study aiming to identify new mechanisms of EAT dysfunction with the potential to become new therapeutic targets in cardiac disease&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a> In particular&#44; application of state-of-the-art high-throughput proteomic methods and their correlation with cardiac function parameters have the potential to open up new paths to the identification of new early surrogate markers of cardiac disease&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Epicardial adipose tissue (dys)function: A new player in heart disease?
(Dis)função do tecido adiposo epicárdico: um novo interveniente nas doenças cardíacas?
Paulo Matafomea,b,c
a University of Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR) and Institute of Physiology, Faculty of Medicine, Coimbra, Portugal
b University of Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), Coimbra, Portugal
c Clinical Academic Center of Coimbra (CACC), Coimbra, Portugal
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to proinflammatory cytokines&#44; chemokines and profibrotic factors of hypertrophic adipocytes &#40;hepatocyte and fibroblast growth factors&#44; transforming growth factor beta&#44; tumor necrosis factor alpha and matrix metalloproteinases&#41;&#46; These conditions are also associated with an imbalance in angiogenic factors&#44; which leads to alterations in vascular architecture&#44; chronic hypoxia&#44; propagation of the proinflammatory milieu and impairment of other adipokines&#44; such as adiponectin&#44; leptin and resistin&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Epicardial adipose tissue &#40;EAT&#41; is located between the visceral layer of the pericardium and the myocardium&#44; while pericardial adipose tissue is located outside the pericardium&#46; Moreover&#44; EAT is irrigated by the coronary circulation&#44; while pericardial adipose tissue is not&#44; and EAT may also be found around coronary arteries&#44; which may directly influence coronary blood flow&#46; This fat depot is especially rich in preadipocytes&#44; rather than mature adipocytes&#44; and shares some features with brown and beige adipocytes&#44; including UCP1 expression and a higher metabolic rate than other fat pads&#46; EAT has a higher capacity for uptake and release of fatty acids&#44; which is important to sustain myocardial metabolism in physiological conditions&#46; Fatty acid flux is regulated by vasoactive factors released by EAT&#44; which control coronary vessel tone&#46; Besides providing fatty acids for cardiomyocyte metabolism&#44; EAT also protects the myocardium through its mechanical and thermogenic properties&#44; preventing changes in myocardial structure and temperature during contraction&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">3</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">EAT is easily detected by common imaging methods such as ultrasonography or computed tomography&#44; which enable its volume to be measured with high accuracy&#46; The relationship between EAT volume and cardiovascular function has been examined in a large number of studies&#46; EAT volume has been correlated with several features of coronary artery disease&#44; including coronary calcification&#44; carotid intima-media thickness and coronary flood flow in patients with coronary artery disease but normal myocardial perfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">4</span></a> EAT volume was also correlated with poorer left ventricular diastolic function&#44; but not other parameters of ventricular function&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">5</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Reduction of EAT volume through physical exercise and sleeve gastrectomy was recently proposed as a promising strategy to reduce atherosclerotic lesions&#44; due to reductions in proinflammatory adipokines and improvement of the inflammatory milieu in the coronary vessel wall&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">6</span></a> Moreover&#44; GLP-1 receptor expression in EAT was recently shown to be linked to genes involved in fatty acid oxidation&#44; and liraglutide was observed to produce a marked decrease in this fat depot&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">7</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">The study of EAT is not a simple task because&#44; besides the fact that its collection requires invasive thoracic surgery&#44; it is not found in rodent models&#46; Moreover&#44; EAT is often obtained from chronic patients undergoing surgery&#44; which does not provide information about early metabolic and endocrine alterations of this fat depot&#46; Thus&#44; factors including difficult access&#44; duration of metabolic or cardiac disease and medication may hamper study of the mechanisms linking EAT &#40;dys&#41;function with cardiac disease&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">The role of other fat depots was initially reported in the context of the pathophysiology of metabolic syndrome&#44; body mass index &#40;BMI&#41; and adiposity being considered the main risk factors for insulin resistance and glucose intolerance&#46; Nowadays&#44; several years after the first studies&#44; there is a growing body of evidence showing that BMI is not a good predictor of metabolic disease&#44; especially insulin resistance&#46; Instead&#44; various studies have reported that adipose tissue dysfunction&#44; with changes in metabolic and endocrine functions&#44; is more closely associated with insulin resistance-associated diseases&#44; such as type 2 diabetes and non-alcoholic fatty liver disease&#46; Thus&#44; EAT can be expected to undergo various changes in metabolic syndrome&#44; which may be related to its greater proatherogenicity&#46; EAT from type 2 diabetic patients was shown to present infiltration of immune cells &#40;including macrophages&#44; T lymphocytes and dendritic cells&#41; and impaired expression of key genes&#44; with a more proinflammatory profile&#46; This inflammatory infiltration creates a proinflammatory environment that extends to the surrounding vessels and cardiomyocytes&#46; The correlation between EAT volume and changes in systolic and diastolic function was observed to be stronger in type 2 diabetic patients than in controls&#44; suggesting that changes occurring in EAT in type 2 diabetes directly impact myocardial function&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">8</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">From an imaging standpoint&#44; good markers of EAT infiltration are necessary&#46; Recently&#44; a study by Liu et al&#46; showed that changes in attenuation&#44; calculated from cardiac computed tomography angiography&#44; are a better predictor of atherosclerosis than EAT volume by itself&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">9</span></a> In molecular terms&#44; impaired EAT secretion of adipokines and profibrotic factors has been observed&#44;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">10</span></a> but little is known regarding the molecular links between EAT &#40;dys&#41;function and cardiovascular function&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Thus&#44; although there is currently some evidence that EAT may be associated with coronary artery disease and other cardiac disease&#44; there is a need for studies able to dissect the molecular links between EAT &#40;dys&#41;function and cardiac disease&#46; In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Mancio et al&#46; describe the protocol of a study aiming to identify new mechanisms of EAT dysfunction with the potential to become new therapeutic targets in cardiac disease&#46;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">11</span></a> In particular&#44; application of state-of-the-art high-throughput proteomic methods and their correlation with cardiac function parameters have the potential to open up new paths to the identification of new early surrogate markers of cardiac disease&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0045" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Revista Portuguesa de Cardiologia (English edition)
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