Figure 1.

The ADBR signaling in the presence of the ligand, which will be blocked by propranolol. According to this model propranolol would decrease de adenylate cyclase activity, decreasing the cAMP (cyclic Adenosine Monophosphate) levels and the activation of PKA (Protein Kinase A). Activation of eNOS (endothelial Nitric-Oxyde Synthase) by PKA will be decreased leading to vasoconstriction. On the other hand, the decrease in PKA activity will affect Src (Proto-oncogene tyrosine-protein kinase Src) expression impairing the HIF-1 (Hypoxia Inducible Factor 1) nuclear translocation with the downregulation of its nuclear targets such as pro-angiogenic genes VEGF (Vascular Endothelial Growth Factor), MMP9 (Matrix Metallopeptidase 9), ENG (Endoglin) and FGF (Fibroblast Growth Factor). The decreased phosphorylation of ERK/MAPK (ERK, Extracellular Signal-Regulated Kinase; MAPK, Mitogen-Activated Protein Kinase) kinases cascade and Src will activate the caspase cascade leading to apoptosis. Created by Biorender.com.