The roles of epicardial adipose tissue in heart failure

Song, Ying; Song, Fei; Wu, Chan; Hong, Yi-Xiang; Li, Gang

doi:10.1007/s10741-020-09997-x

Cited by 27 publications

(15 citation statements)

References 92 publications

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“…Epicardial adipose tissue (EAT) has been noticed to regulate adipogenesis, insulin resistance, renin angiotensin-aldosterone system (RAAS), cardiac remodeling and output, by which it facilitates physiological and pathophysiological processes of coronary failure. Through paracrine, endocrine and vasocrine pathways, EAT secretes a wide range of adipokines, adrenomedullin, miRNA and adiponectin related to the progress of cardiovascular disease via intracellular and extracellular mechanisms [ 9 ]. A study on the protective effects of safflower oil against metabolic syndrome (MS), was carried out on 67 patients, given 8 g of safflower or placebo daily for 12 weeks.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin System (Rescue Hormone): The Missing Link between Metabolic and Cardiovascular Diseases

Aljafary

Al-Suhaimi

2022

Pharmaceutics

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The adipose tissue, regardless of its role in generating and storing energy, acts as a key player as an endocrine tissue, producing a wide scale of cytokines/hormones called adipokines. Adipokines such as leptin, resistin, visfatin and osteopontin own pro-inflammatory effects on the cardiovascular system in some cases. In contrast, some adipokines have cardioprotective and anti-inflammatory impacts including adiponectin, omentin, and apelin. One of the key adipokines is adiponectin, the abundant peptide regulating hormone that is released mainly by adipocytes and cardiomyocytes as well as by endothelial and skeletal cells. It acts through two main receptors: AdipoR1 and AdipoR2, forming the “Adiponectin system” which effectively exerts its cellular mechanisms and responses in target cells. It regulates various metabolic processes, while adiponectin is the adipocyte hormone known for its cardioprotective impact in clinical and experimental research. It is also a well-effector metabolic adipokine, since weight loss or diet restriction show a link with rises in adiponectin concentrations, which is accompanied with increasing insulin sensitivity, glucose, and lipids-regulation via adiponectin’s antioxidant, anti-inflammatory, anti-fibrotic actions. The high adiponectin level made it an attractive player in developing therapeutical treatments for metabolic syndromes and cardiovascular disease. The elevated plasma levels of adiponectin are mostly attributed to its benefits on cardio-metabolism. In some cases, adiponectin has been paradoxically accompanied with elevated risk of cardiovascular disease, so higher adiponectin concentration is a marker of poor prediction. Thus, the adiponectin system is attractive to researchers as a biomarker of heart disease advancement and a predictor of prognosis during the term of some cardiovascular diseases and its mechanical functions in Hypertension and diabetic patients. This review highlights the physiological roles of adiponectin as an anti-inflammatory and cardioprotective hormone as well as how it plays as a biomarker and potential therapeutic tool in the cardiovascular system in adult, children, and adolescents. The adiponectin system may be seen as a rescue hormone aiding in remodeling of the cardiovascular system on both cellular and molecular levels. The paradox role of adiponectin relevant to cardiovascular mortality should be taken into consideration.

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Section: Introductionmentioning

confidence: 99%

Adiponectin System (Rescue Hormone): The Missing Link between Metabolic and Cardiovascular Diseases

Aljafary

Al-Suhaimi

2022

Pharmaceutics

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“…In this context, a study by Zou et al identified miR-410-5p and its promoting effects on cardiac fibrosis in mice with regular diets by silencing Smad7; concurrently, miR-410-5p demonstrated anti-fibrotic effects in mice fed high-fat diets (193). These results suggest a dual role for miRNAs in cardiovascular pathologies; besides the cardioprotective role of some miRNAs, these molecules can exert harmful effects on cardiac tissue, promoting effects such as local inflammation, hypertrophy, remodeling and cardiac fibrosis in different CVDs (183,(194)(195)(196)(197)(198). Cardiokines: stimuli such as cardiac ischemia, reperfusion, oxidative and hemodynamic stress stimulate the production of cardiokines, which signaling in an endocrine and paracrine mechanism to the adipose tissue promoting weight loss by increasing thermogenesis and both the release and oxidation of fatty acids.…”

Section: Mirnas and Evsmentioning

confidence: 84%

“…identified miR-410-5p and its promoting effects on cardiac fibrosis in mice with regular diets by silencing Smad7; concurrently, miR-410-5p demonstrated anti-fibrotic effects in mice fed high-fat diets ( 193 ). These results suggest a dual role for miRNAs in cardiovascular pathologies; besides the cardioprotective role of some miRNAs, these molecules can exert harmful effects on cardiac tissue, promoting effects such as local inflammation, hypertrophy, remodeling and cardiac fibrosis in different CVDs ( 183 , 194 – 198 ).…”

Section: Intercellular Signaling Between Adipocytes and Myocardial Cellsmentioning

confidence: 94%

“…Most miRNAs on EAT operate through autocrine fashion and have been implicated in various AT processes such as adipocyte differentiation, fatty acid metabolism, cholesterol homeostasis, adipogenesis, browning and inflammation (183)(184)(185). Other miRNAs are released into the circulation via exosomes, from where they travel to and penetrate the heart or other distant organs (186).…”

Section: Mirnas and Evsmentioning

confidence: 99%

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The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium

et al. 2021

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Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.

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“…Numerous pathogenic factors are associated with the development and progression of heart failure, including accumulated adipose tissue and fatty acids. In recent years, the epicardial adipose tissue (EAT) has gained much attention due to its localization in the heart and versatile functions [ 82 , 83 , 84 ]. Under physiological conditions, the EAT fulfills cardioprotective functions e.g., by the secretion of anti-inflammatory and anti-atherosclerotic cytokines such as adiponectin and adrenomedullin [ 85 , 86 ].…”

Section: Lipotoxicity and Mitochondrial Homeostasismentioning

confidence: 99%

Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium

Kretzschmar

Schulze

2021

IJMS

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Heart failure remains the most common cause of death in the industrialized world. In spite of new therapeutic interventions that are constantly being developed, it is still not possible to completely protect against heart failure development and progression. This shows how much more research is necessary to understand the underlying mechanisms of this process. In this review, we give a detailed overview of the contribution of impaired mitochondrial dynamics and energy homeostasis during heart failure progression. In particular, we focus on the regulation of fatty acid metabolism and the effects of fatty acid accumulation on mitochondrial structural and functional homeostasis.

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The roles of epicardial adipose tissue in heart failure

Cited by 27 publications

References 92 publications

Adiponectin System (Rescue Hormone): The Missing Link between Metabolic and Cardiovascular Diseases

Adiponectin System (Rescue Hormone): The Missing Link between Metabolic and Cardiovascular Diseases

The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium

Mitochondrial Homeostasis Mediates Lipotoxicity in the Failing Myocardium

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