Human epicardial adipose tissue inflammation correlates with coronary artery disease

Fan, Wenjun; Si, Yueqiao; Xing, Enhong; Feng, Zengbin; Ding, Zhenjiang; Liu, Yixiang; Wei, Chen; Tian, Yanan; Zhang, Ying; Liu, Jingyi; Sun, Lixian

doi:10.1016/j.cyto.2022.156119

Cited by 11 publications

(7 citation statements)

References 47 publications

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“…These findings suggest that adiponectin and HOMA-IR could explain the increased cardiovascular risk associated with VAT. These results align with the hypothesis proposed by Reyes-Barrera J. et al, and Fan W. et al suggesting that excessive production of free fatty acids and pro-inflammatory cytokines by ectopic fat depots may promote local damage, which leads to adipose tissue dysfunction [15,16]. Additionally, in a previous report, we described that more than the excess in free fatty acids is the decreased concentration of circulating adiponectin, which explains the systemic IR, particularly among high VAT subjects [30].…”

Section: Physiopathological Mechanism Related To the Association Of V...supporting

confidence: 91%

“…However, post-mortem studies [ 10 ] and other analyses carried out in prospective cohorts in which the development of imaging techniques has allowed the identification and quantification of ectopic fat deposits suggest that visceral abdominal fat (VAT) [ 11 , 12 ] and pericardial fat [ 13 , 14 ] are responsible for cardiovascular risk related to adiposity. On the other hand, it has also been suggested that subcutaneous adipose tissue dysfunction, characterized by insulin resistance, low plasma adiponectin, and increased ectopic fat deposits, is the initial damage that promotes CAD development [ 15 , 16 ]. Moreover, it has been observed that body fat is a pathophysiological modulator related to the incidence and progression of CAC [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

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Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study

Antonio-Villa

Juárez-Rojas

Posadas-Sánchez

et al. 2023

Cardiovasc Diabetol

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Background Coronary artery calcium (CAC) improves cardiovascular event prediction. Visceral adipose tissue (VAT) is a cardiometabolic risk factor that may directly or through its related comorbidities determine the obesity-related risk. A clinical VAT estimator could allow an efficient evaluation of obesity-related risk. We aimed to analyze the effect of VAT and its related cardiometabolic risk factors on CAC progression. Methods CAC was quantified at baseline and after 5 years by computed tomography (CT), determining its progression. VAT and pericardial fat were measured by CT and estimated by a clinical surrogate (METS-VF). Considered cardiometabolic risk factors were: peripheral insulin resistance (IR), HOMA-IR, adipose tissue IR (ADIPO-IR), and adiponectin. Factors independently associated to CAC progression were analyzed by adjusted Cox proportional hazard models, including statin use and ASCVD risk score as covariates. We performed interaction and mediation models to propose possible pathways for CAC progression. Results The study included 862 adults (53 ± 9 years, 53% women), incidence CAC progression rate: 30.2 (95% CI 25.3–35.8)/1000 person-years. VAT (HR: 1.004, 95% CI 1.001–1.007, p < 0.01) and METS-VF (HR: 1.001, 95% CI 1.0–1.001, p < 0.05) independently predicted CAC progression. VAT-associated CAC progression risk was evident among low-risk ASCVD subjects, and attenuated among medium–high-risk subjects, suggesting that traditional risk factors overcome adiposity in the latter. VAT mediates 51.8% (95% CI 44.5–58.8%) of the effect attributable to IR together with adipose tissue dysfunction on CAC progression. Conclusions This study supports the hypothesis that VAT is a mediator of the risk conferred by subcutaneous adipose tissue dysfunction. METS-VF is an efficient clinical surrogate that could facilitate the identification of at-risk adiposity subjects in daily clinical practice.

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Section: Physiopathological Mechanism Related To the Association Of V...supporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study

Antonio-Villa

Juárez-Rojas

Posadas-Sánchez

et al. 2023

Cardiovasc Diabetol

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“…This is in line with the different origin and vascularization of PAT (2, 7). Lower CD206 expression in EAT and SAT might be important because in concomitance with atherosclerosis progression the number of M2 macrophages in the plaques decreases (32) in various tissues including AT, with consequent formation of crown-like structures, a typical hallmark of chronic fat tissue inflammation that possibly hints CHD (33). We found NOS2 to be less expressed in EAT with respect to the other compartments, although statistical significance was reached only compared to SAT in the control group.…”

Section: Discussionmentioning

confidence: 55%

Macrophage polarization markers in subcutaneous, pericardial, and epicardial adipose tissue are altered in patients with coronary heart disease

Papotti

Opstad²,

Åkra³

et al. 2023

Front. Cardiovasc. Med.

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BackgroundEpicardial and pericardial adipose tissue (EAT and PAT) surround and protect the heart, with EAT directly sharing the microcirculation with the myocardium, possibly presenting a distinct macrophage phenotype that might affect the inflammatory environment in coronary heart disease (CHD). This study aims to investigate the expression of genes in different AT compartments driving the polarization of AT macrophages toward an anti-inflammatory (L-Galectin 9; CD206) or pro-inflammatory (NOS2) phenotype.MethodsEAT, PAT, and subcutaneous (SAT) biopsies were collected from 52 CHD patients undergoing coronary artery bypass grafting, and from 22 CTRLs undergoing aortic valve replacement. L-Galectin9 (L-Gal9), CD206, and NOS2 AT gene expression and circulating levels were analyzed through RT-PCR and ELISA, respectively.ResultsL-Gal9, CD206, and NOS2 gene expression was similar in all AT compartments in CHD and CTRLs, as were also L-Gal9 and CD206 circulating levels, while NOS2 serum levels were higher in CHD (p = 0.012 vs. CTRLs). In CTRLs, NOS2 expression was lower in EAT vs. SAT (p = 0.007), while in CHD patients CD206 expression was lower in both SAT and EAT as compared to PAT (p = 0.003, p = 0.006, respectively), suggestive of a possible macrophage reprogramming toward a pro-inflammatory phenotype in EAT. In CHD patients, NOS2 expression in SAT correlated to that in PAT and EAT (p = 0.007, both), CD206 expression correlated positively to L-Gal9 (p < 0.001) only in EAT, and CD206 expression associated with that of macrophage identifying markers in all AT compartments (p < 0.001, all). In CHD patients, subjects with LDL-C above 1.8 mmol/L showed significantly higher NOS2 expression in PAT and EAT as compared to subjects with LDL-C levels below (p < 0.05), possibly reflecting increased cardiac AT pro-inflammatory activation. In SAT and PAT, CD206 expression associated with BMI in both CHD and CTRLs (p < 0.05, all), and with L-Gal9 in EAT, however only in CTRLs (p = 0.002).ConclusionCHD seems to be accompanied by an altered cardiac, and especially epicardial AT macrophage polarization. This may represent an important pathophysiological mechanism and a promising field of therapy targeting the excessive AT inflammation, in need of further investigation.

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“…Unfortunately, the data concerning CLS formation in EAT are currently limited. Inflammatory cell infiltration in EAT from individuals with CAD is higher than in SAT [57]. The accumulation of mast cells, which secrete multiple vasoactive molecules, may contribute to the rupture of vulnerable plaque.…”

Section: The Role Of Inflammationmentioning

confidence: 90%

“…Moreover, mast cells can activate T lymphocytes. CAD is associated with increased infiltration rates of EAT by T lymphocytes (CD3+) and B lymphocytes (CD20+) [57,59]. However, little is known about the impact of lymphocytes located in EAT on ACS development.…”

Section: The Role Of Inflammationmentioning

confidence: 99%

The Role of Epicardial Adipose Tissue in Acute Coronary Syndromes, Post-Infarct Remodeling and Cardiac Regeneration

Krauz,

Kempiński,

Jańczak

et al. 2024

IJMS

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Epicardial adipose tissue (EAT) is a fat deposit surrounding the heart and located under the visceral layer of the pericardium. Due to its unique features, the contribution of EAT to the pathogenesis of cardiovascular and metabolic disorders is extensively studied. Especially, EAT can be associated with the onset and development of coronary artery disease, myocardial infarction and post-infarct heart failure which all are significant problems for public health. In this article, we focus on the mechanisms of how EAT impacts acute coronary syndromes. Particular emphasis was placed on the role of inflammation and adipokines secreted by EAT. Moreover, we present how EAT affects the remodeling of the heart following myocardial infarction. We further review the role of EAT as a source of stem cells for cardiac regeneration. In addition, we describe the imaging assessment of EAT, its prognostic value, and its correlation with the clinical characteristics of patients.

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Human epicardial adipose tissue inflammation correlates with coronary artery disease

Cited by 11 publications

References 47 publications

Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study

Visceral adipose tissue is an independent predictor and mediator of the progression of coronary calcification: a prospective sub-analysis of the GEA study

Macrophage polarization markers in subcutaneous, pericardial, and epicardial adipose tissue are altered in patients with coronary heart disease

The Role of Epicardial Adipose Tissue in Acute Coronary Syndromes, Post-Infarct Remodeling and Cardiac Regeneration

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