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The adipose-neural axis is involved in epicardial adipose tissue-related cardiac arrhythmias.
Cell Rep Med
May 2024
Center for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China; National-Local Joint Engineering Research Center for Stem Cells and Regenerative Medicine, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China; Department of Histoembryology and Cell Biology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, China; Guangdong Key Laboratory of Reproductive Medicine, Guangzhou, Guangdong, China. Electronic address:
Dysfunction of the sympathetic nervous system and increased epicardial adipose tissue (EAT) have been independently associated with the occurrence of cardiac arrhythmia. However, their exact roles in triggering arrhythmia remain elusive. Here, using an in vitro coculture system with sympathetic neurons, cardiomyocytes, and adipocytes, we show that adipocyte-derived leptin activates sympathetic neurons and increases the release of neuropeptide Y (NPY), which in turn triggers arrhythmia in cardiomyocytes by interacting with the Y1 receptor (Y1R) and subsequently enhancing the activity of the Na/Ca exchanger (NCX) and calcium/calmodulin-dependent protein kinase II (CaMKII).
View Article and Find Full Text PDFInvolvement of pyroptosis pathway in epicardial adipose tissue - myocardium axis in experimental heart failure with preserved ejection fraction.
Biochem Biophys Res Commun
December 2022
Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, Nanjing, China. Electronic address:
Epicardial adipose tissue (EAT) is a metabolically active organ which generates inflammatory cytokines. Thickness of EAT is associated with onset and development of heart failure with preserved ejection fraction (HFpEF). However, it is still unclear the specific mechanisms and pharmacological targets on EAT induced inflammation in HFpEF.
View Article and Find Full Text PDFEpicardial Adipocyte-derived TNF-α Modulates Local Inflammation in Patients with Advanced Coronary Artery Disease.
Curr Vasc Pharmacol
May 2022
Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Center Ljubljana, Zaloska 7, 1000, Ljubljana, Slovenia.
Epicardial Adipocyte-derived TNF-α Modulates Local Inflammation in Patients with Advanced Coronary Artery Disease.
Curr Vasc Pharmacol
May 2022
Department of Cardiac Surgery, Euroclinic of Athens, Athens, Greece.
Background: Epicardial Adipose Tissue (EAT) surrounds the epicardium and can mediate harmful effects related to Coronary Artery Disease (CAD).
Objective: We explored the regional differences between adipose stores surrounding diseased and non-diseased segments of coronary arteries in patients with advanced CAD.
Methods: We enrolled 32 patients with known CAD who underwent coronary artery bypass graft (CABG) surgery.
Hypertrophic Adipocyte-Derived Exosomal miR-802-5p Contributes to Insulin Resistance in Cardiac Myocytes Through Targeting HSP60.
Obesity (Silver Spring)
October 2020
Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China.
Objective: This study aimed to elucidate the mechanism by which hypertrophic adipocytes regulate insulin signaling in cardiac myocytes.
Methods: Palmitate was used to induce hypertrophic 3T3-L1 adipocytes. Exosomes were purified from normal control or hypertrophic 3T3-L1 adipocyte-associated conditioned medium.
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