Proteostasis in epicardial versus subcutaneous adipose tissue in heart failure subjects with and without diabetes

Burgeiro, Ana; Fonseca, Ana; Espinoza, Daniel; Carvalho, Luana Martins de; Lourenço, Nuno; Antunes, M.; Carvalho, Eugénia

doi:10.1016/j.bbadis.2018.03.025

Cited by 10 publications

(6 citation statements)

References 117 publications

(126 reference statements)

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“…Few studies have looked into autophagy activity in EAT. In one study comparing EAT and SAT samples from heart failure patients, EAT was found to have higher expression of genes related to autophagy and mitophagy (selective autophagy of the mitochondria), as well as protein expression related to autophagy (Beclin-1 and microtubule-associated proteins 1A/1B light chain 3B (LC3B-II)) (Burgeiro et al, 2018).…”

Section: Types Of Fat and Arrhythmia Developmentmentioning

confidence: 99%

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

et al. 2018

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Obesity and atrial fibrillation have risen to epidemic levels worldwide and may continue to grow over the next decades. Emerging evidence suggests that obesity promotes atrial and ventricular arrhythmias. This has led to trials employing various strategies with the ultimate goal of decreasing the atrial arrhythmic burden in obese patients. The effectiveness of these interventions remains to be determined. Obesity is defined by the expansion of adipose mass, making adipocytes a prime candidate to mediate the pro-arrhythmogenic effects of obesity. The molecular mechanisms linking obesity and adipocytes to increased arrhythmogenicity in both the atria and ventricles remain poorly understood. In this focused review, we highlight areas of potential molecular interplay between adipocytes and cardiomyocytes. The effects of adipocytes may be direct, local or remote. Direct effect refers to adipocyte or fatty infiltration of the atrial and ventricular myocardium itself, possibly causing increased dispersion of normal myocardial electrical signals and fibrotic substrate of adipocytes that promote reentry or adipocytes serving as a direct source of aberrant signals. Local effects may originate from nearby adipose depots, specifically epicardial adipose tissue (EAT) and pericardial adipose tissue, which may play a role in the secretion of adipokines and chemokines that can incite inflammation given the direct contact and disrupt the conduction system. Adipocytes can also have a remote effect on the myocardium arising from their systemic secretion of adipokines, cytokines and metabolites. These factors may lead to mitochondrial dysfunction, oxidative stress, autophagy, mitophagy, autonomic dysfunction, and cardiomyocyte death to ultimately produce a pro-arrhythmogenic state. By better understanding the molecular mechanisms connecting dysfunctional adipocytes and arrhythmias, novel therapies may be developed to sever the link between obesity and arrhythmias.

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Section: Types Of Fat and Arrhythmia Developmentmentioning

confidence: 99%

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

et al. 2018

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“…The vasocrine way includes the direct transit of free fatty acids and adipokines into the coronary lumen's vasa vasorum [31]. The adipocytokines mentioned above activate adenosine monophosphate-activated protein kinase (AMPK), an enzyme mostly produced by heart and skeletal muscles [32,33]. Under cellular stress states and low energy supplies, AMPK induces catabolic pathways and restricts anabolic ones in order to increase cellular adenosine triphosphate (ATP) levels and regulates glucose and free fatty acid uptake [32,33].…”

Section: Epicardial Adipose Tissue As An Endocrine Organmentioning

confidence: 99%

“…Epicardial adipocytes are generally characterized by lower levels of glucose transporter type 4 (GLUT-4) [32]. However, in diabetic individuals also suffering from coronary atherosclerosis, GLUT4 levels in EAT were even lower, underlying in this way the local role of insulin-induced atherogenesis in CAD [62].…”

Section: Epicardial Adipose Tissue and Coronary Artery Diseasementioning

confidence: 99%

Epicardial Adipose Tissue as an Independent Cardiometabolic Risk Factor for Coronary Artery Disease

Karampetsou¹,

Alexopoulos²,

Minia³

et al. 2022

Cureus

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During the last decades, visceral adiposity has been at the forefront of scientific research because of its complex role in the pathogenesis of cardiovascular diseases. Epicardial adipose tissue (EAT) is the visceral lipid compartment between the myocardium and the visceral pericardium. Due to their unobstructed anatomic vicinity, epicardial fat and myocardium are nourished by the same microcirculation. It is widely known that EAT serves as an energy lipid source and thermoregulator for the human heart. In addition to this, epicardial fat exerts highly protective effects since it releases a great variety of anti-inflammatory molecules to the adjacent cardiac muscle. Taking into account the unique properties of human EAT, it is undoubtedly a key factor in cardiac physiology since it facilitates complex heart functions. Under pathological circumstances, however, epicardial fat promotes coronary atherosclerosis in a variety of ways. Therefore, the accurate estimation of epicardial fat thickness and volume could be utilized as an early detecting method and future medication target for coronary artery disease (CAD) elimination. Throughout the years, several therapeutic approaches for dysfunctional human EAT have been proposed. A balanced healthy diet, aerobic and anaerobic physical activity, bariatric surgery, and pharmacological treatment with either traditional or novel antidiabetic and antilipidemic drugs are some of the established medical approaches. In the present article, we review the current knowledge regarding the anatomic and physiological characteristics of epicardial fat. In addition to this, we describe the pathogenic mechanisms which refer to the crosstalk between epicardial fat alteration and coronary arterial atherosclerosis development. Lastly, we present both lifestyle and pharmacological methods as possible treatment options for EAT dysfunction.

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“…cardiomyopathies). 101 Burgeiro et al demonstrated that both the unfolded protein response (e.g. inositol-requiring enzyme 1α, glucose-regulated protein 94 KDa, glucose-regulated protein 78 KDa) and the autophagy pathways were significantly increased in EAT compared with SC AT.…”

Section: Eat and Pat As Predictors Of Cvd Riskmentioning

confidence: 99%

“…inositol-requiring enzyme 1α, glucose-regulated protein 94 KDa, glucose-regulated protein 78 KDa) and the autophagy pathways were significantly increased in EAT compared with SC AT. 101…”

Section: Eat and Pat As Predictors Of Cvd Riskmentioning

confidence: 99%

Can We Decrease Epicardial and Pericardial Fat in Patients With Diabetes?

Muzurović

Vujosevic

Mikhailidis

2021

J Cardiovasc Pharmacol Ther

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Diabetes mellitus (DM) is a chronic and complex metabolic disorder and also an important cause of cardiovascular (CV) disease (CVD). Patients with type 2 DM (T2DM) and obesity show a greater propensity for visceral fat deposition (and excessive fat deposits elsewhere) and the link between adiposity and CVD risk is greater for visceral than for subcutaneous (SC) adipose tissue (AT). There is growing evidence that epicardial AT (EAT) and pericardial AT (PAT) play a role in the development of DM-related atherosclerosis, atrial fibrillation (AF), myocardial dysfunction, and heart failure (HF). In this review, we will highlight the importance of PAT and EAT in patients with DM. We also consider therapeutic interventions that could have a beneficial effect in terms of reducing the amount of AT and thus CV risk. EAT is biologically active and a likely determinant of CV morbidity and mortality in patients with DM, given its anatomical characteristics and proinflammatory secretory pattern. Consequently, modification of EAT/PAT may become a therapeutic target to reduce the CV burden. In patients with DM, a low calorie diet, exercise, antidiabetics and statins may change the quantity of EAT, PAT or both, alter the secretory pattern of EAT, improve the metabolic profile, and reduce inflammation. However, well-designed studies are needed to clearly define CV benefits and a therapeutic approach to EAT/PAT in patients with DM.

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Proteostasis in epicardial versus subcutaneous adipose tissue in heart failure subjects with and without diabetes

Abstract: UPR and autophagy are increased in EAT compared to SAT, opening doors to the identification of early biomarkers for cardiomyopathies and novel therapeutic targets.

Cited by 10 publications

References 117 publications

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

Linking Arrhythmias and Adipocytes: Insights, Mechanisms, and Future Directions

Epicardial Adipose Tissue as an Independent Cardiometabolic Risk Factor for Coronary Artery Disease

Can We Decrease Epicardial and Pericardial Fat in Patients With Diabetes?

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