Browning Epicardial Adipose Tissue: Friend or Foe?

Doukbi, Elisa; Soghomonian, Astrid; Sengenès, Coralie; Ahmed, Shaista; Ancel, Patricia; Dutour, Anne; Gaborit, Bénédicte

doi:10.3390/cells11060991

Cited by 22 publications

(16 citation statements)

References 228 publications

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“…The PGC-1 α is a member of the PGC-1 family that regulates adaptive thermogenesis and mitochondrial function [ 35 ]. PGC-1 α can be directly activated by p38 MAPK [ 36 ] and participates in the elimination of ROS in the heart [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4–PGC-1α–PPARα/PPARγ Signaling in Isolated Beating Rat Atria

Han

Lin

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Atrial natriuretic peptide (ANP), a canonical cardiac hormone, is mainly secreted from atrial myocytes and is involved in the regulation of body fluid, blood pressure homeostasis, and antioxidants. Cholecystokinin (CCK) is also found in cardiomyocytes as a novel cardiac hormone and induces multiple cardiovascular regulations. However, the direct role of CCK on the atrial mechanical dynamics and ANP secretion is unclear. The current study was to investigate the effect of CCK octapeptide (CCK-8) on the regulation of atrial dynamics and ANP secretion. Experiments were performed in isolated perfused beating rat atria. ANP was measured using radioimmunoassay. The levels of hydrogen peroxide (H2O2) and arachidonic acid (AA) were determined using ELISA Kits. The levels of relative proteins and mRNA were detected by Western blot and RT-qPCR. The results showed that sulfated CCK-8 (CCK-8s) rather than desulfated CCK-8 increased the levels of phosphorylated cytosolic phospholipase A2 and AA release through activation of CCK receptors. This led to the upregulation of NADPH oxidase 4 (NOX4) expression levels and H2O2 production and played a negative inotropic effect on atrial mechanical dynamics via activation of ATP-sensitive potassium channels and large-conductance calcium-activated potassium channels. In addition, CCK-8s-induced NOX4 subsequently upregulated peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) expression levels through activation of p38 mitogen-activated protein kinase as well as the serine/threonine kinase signaling, ultimately promoting the secretion of ANP via activation of PPARα and PPARγ. In the presence of the ANP receptor inhibitor, the CCK-8-induced increase of AA release, H2O2 production, and the upregulation of NOX4 and CAT expressions was augmented but the SOD expression induced by CCK-8s was repealed. These findings indicate that CCK-8s promotes the secretion of ANP through activation of NOX4–PGC-1α–PPARα/PPARγ signaling, in which ANP is involved in resistance for NOX4 expression and ROS production and regulation of SOD expression.

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Section: Discussionmentioning

confidence: 99%

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4–PGC-1α–PPARα/PPARγ Signaling in Isolated Beating Rat Atria

Han

Lin

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…However, on a histological basis, EAT appears more like white adipose tissue. Nonetheless, the induction of UCP1 in EAT is an intriguing concept to combat the development of cardiovascular disease associated with EAT ( 74 ).…”

Section: Implications For Treatment and Future Directionsmentioning

confidence: 99%

Epicardial adipocytes in the pathogenesis of atrial fibrillation: An update on basic and translational studies

2023

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Epicardial adipose tissue (EAT) is an endocrine organ containing a host of cell types and undoubtedly serving a multitude of important physiologic functions. Aging and obesity cause hypertrophy of EAT. There is great interest in the possible connection between EAT and cardiovascular disease, in particular, atrial fibrillation (AF). Increased EAT is independently associated with AF and adverse events after AF ablation (e.g., recurrence of AF, and stroke). In general, the amount of EAT correlates with BMI or visceral adiposity. Yet on a molecular level, there are similarities and differences between epicardial and abdominal visceral adipocytes. In comparison to subcutaneous adipose tissue, both depots are enriched in inflammatory cells and chemokines, even in normal conditions. On the other hand, in comparison to visceral fat, epicardial adipocytes have an increased rate of fatty acid release, decreased size, and increased vascularity. Several studies have described an association between fibrosis of EAT and fibrosis of the underlying atrial myocardium. Others have discovered paracrine factors released from EAT that could possibly mediate this association. In addition to the adjacent atrial cardiomyocytes, EAT contains a robust stromal-vascular fraction and surrounds the ganglionic plexi of the cardiac autonomic nervous system (cANS). The importance of the cANS in the pathogenesis of atrial fibrillation is well known, and it is quite likely that there is feedback between EAT and the cANS. This complex interplay may be crucial to the maintenance of normal sinus rhythm or the development of atrial fibrillation. The extent the adipocyte is a microcosm of metabolic health in the individual patient may determine which is the predominant rhythm.

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“…Эпикардиальные адипоциты меньше адипоцитов в подкожных и других висцеральных жировых отложениях из-за большего количества преадипоцитов по сравнению со зрелыми адипоцитами. ЭЖТ составляет 20% массы сердца и 1% от общей жировой массы в физиологических условиях [5].…”

Section: роль эпикардиального жира в физиологии сердца в норме и при ...unclassified

“…Физиологически ЭЖТ играет кардиопротекторную роль, обеспечивая механическую защиту, служит источником энергии для миокарда и одновременно буфером, защищающим от липотоксичности при избытке свободных жирных кислот (СЖК). ЭЖТ вырабатывает противовоспалительные адипокины, в частности адипонектин и адреномедуллин, обладающие антиатеросклеротическими и противовоспалительными свойствами [5]. Белок, связывающий жирные кислоты адипоцитов (также известный как FABP4), который высоко экспрессируется в ЭЖТ, участвует во внутриклеточном транспорте жирных кислот из ЭЖ в миокард [6].…”

Section: роль эпикардиального жира в физиологии сердца в норме и при ...unclassified

Recent assessment methods of epicardial adipose tissue

Vasilkova

T.A.

2023

SJCEM

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Epicardial adipose tissue (EAT) is a visceral depot of the heart fat, which has high plasticity and directly contact with the myocardium and coronary arteries. Epicardial fat is a unique paracrine organ closely anatomically and physiologically related to the myocardium. Recent studies have repeatedly confirmed the role of epicardial fat in the progression of the cardiovascular diseases. The accumulation of EAT, measured by using new non-invasive imaging techniques, is prospectively associated with the onset and progression of coronary heart disease (CHD) and atrial fibrillation. This review focuses on modern in vivo methods for assessing epicardial fat.

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Browning Epicardial Adipose Tissue: Friend or Foe?

Cited by 22 publications

References 228 publications

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4–PGC-1α–PPARα/PPARγ Signaling in Isolated Beating Rat Atria

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4–PGC-1α–PPARα/PPARγ Signaling in Isolated Beating Rat Atria

Epicardial adipocytes in the pathogenesis of atrial fibrillation: An update on basic and translational studies

Recent assessment methods of epicardial adipose tissue

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