التفاصيل البيبلوغرافية
| العنوان: |
New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review. |
| المؤلفون: |
Jalil, Jorge E., Gabrielli, Luigi, Ocaranza, María Paz, MacNab, Paul, Fernández, Rodrigo, Grassi, Bruno, Jofré, Paulina, Verdejo, Hugo, Acevedo, Monica, Cordova, Samuel, Sanhueza, Luis, Greig, Douglas |
| المصدر: |
International Journal of Molecular Sciences; Apr2024, Vol. 25 Issue 8, p4407, 24p |
| مصطلحات موضوعية: |
GLUCAGON-like peptide-1 receptor, TYPE 2 diabetes, EPICARDIAL adipose tissue, METABOLIC syndrome, HEART failure, INSULIN, ADIPOGENESIS, GLUCAGON receptors |
| مستخلص: |
This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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