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Table 2 Compilation of the most important results of GLP-1 and GLP-1R agonists from animal studies mentioned in the text

From: Cardiovascular effects of Glucagon-like peptide 1 (GLP-1) receptor agonists

 

GLP-1

References

GLP-1R agonist

References

 

Elicits cAMP in mouse cardiomyocytes

[38]

mRNAExpression is localized in cardiac atria and and its activation promotes secretion of atrial natriuretic peptide and increases BP.

[11],[31],[64]

 

Inhibits palmitate- and ceramide-induced phosphatidylserine exposure and DNA fragmentation

[44]

Acts via cAMP in endosome

[37]

 

Increases myocardial glucose uptake in dogs

[46]

Decreases myocyte apoptosis by activation of cAMP/PKA/CREB pathway

[39]

 

May preserve cardiomyocyte viability, increases metabolic efficiency and inhibits the structural and functional remodeling after myocardial infarction.

[49]

Induces cardiomyocyte growth and activation of glucose metabolism by a mechanism envolving AKT and ERK phosphorylations

[24],[40],[41]

Animals studies

Increases systolic and diatolic BP, as well as HR im male rats acutely.

[52]

Has cardioprotective functions related to inhibition of cardiomyocytes apoptosis due their ROS scanvenger actions, by increasing endogenous antioxidant defenses.

[42]

 

Inhibts glucagon release by a mechanism PKA dependent and glucose independent

[16],[17]

Cardioprotective functions are mediated by PI3K and partially dependent on ERK1/2

[43]

 

Decreases contractility in primary culture of adult rat cardiomyocytes and in isolated rat hearts

[45],[76]

Attenuates atherosclerotic lesions by reducing monocyte/macrophage accumulation in the arterialwall and inhibits the inflammatory response in macrophages.

[65]

   

Reduces the inflammatory markers: MCP-1 and TNF- α in response to lipopolysaccharide in cultured peritoneal macrophages harvested from mice.

[66]

   

Reduces monocyte adhesion to aortic endothelial cells and atheroscleroticlesion size in nondiabetic C57BL/6 and ApoE-/- mice.

[65]