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Titlebook: Epicardial Adipose Tissue; From Cell to Clinic Gianluca Iacobellis Book 2020 Springer Nature Switzerland AG 2020 Cardiovascular risk and ep

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樓主: Kennedy
41#
發(fā)表于 2025-3-28 15:17:49 | 只看該作者
V. N. Chukanov,B. A. Korobitsintery disease (CAD), as emerged only recently. The mechanisms through which epicardial fat can cause atherosclerosis are complex and multifactorial. Its anatomical proximity to the heart, the unique transcriptome, and intense proteasome are the major atherogenic factors of the epicardial adipose tiss
42#
發(fā)表于 2025-3-28 22:49:02 | 只看該作者
43#
發(fā)表于 2025-3-29 01:06:49 | 只看該作者
44#
發(fā)表于 2025-3-29 04:26:26 | 只看該作者
Budgetary Constraints on Doctrinal Concepts,le, although results are not univocal. Experimental studies suggest a potential protective role of the brown fat features of EAT against the systolic heart failure. A function of EAT p53 and adiponectin has been also suggested in patients with heart failure. A neuromodulatory role of EAT in heart fa
45#
發(fā)表于 2025-3-29 09:45:58 | 只看該作者
46#
發(fā)表于 2025-3-29 11:29:01 | 只看該作者
,Test and Assessment of Air Purifier [1–2],iver infiltration and insulin resistance. EAT has shown to correlate and predict the risk of developing the metabolic syndrome, although there is no consensus on the EAT threshold risk values, yet. Higher EAT is associated with higher cardiometabolic risk, independently of traditional risk markers.
47#
發(fā)表于 2025-3-29 17:51:40 | 只看該作者
https://doi.org/10.1007/978-3-0348-7970-5aldosterone can lead to accumulation of epicardial adipose tissue (EAT), interfering with functional state. In fact, increased mineralocorticoid signaling is critically involved in the secretion of proinflammatory cytokines by EAT with consequent profibrotic cascade activation in the myocardium. In
48#
發(fā)表于 2025-3-29 19:47:36 | 只看該作者
49#
發(fā)表于 2025-3-30 03:39:06 | 只看該作者
50#
發(fā)表于 2025-3-30 06:36:26 | 只看該作者
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