Fig. 3
From: Targeting endothelial cell metabolism for cardio-protection from the toxicity of antitumor agents
Metabolic pathways preserving EC function. ECs maintain a prosurvival phenotype through the upregulation of eNOS, the activation of cGMP, Akt and MAPK pathways, and the transcription of FGF-2. ACEi, PKCε activators, novel NO donor drugs, VEGF mimetic peptides and ALDH2 activator have been reported to modulate eNOS activity and/or FGF-2 expression, suggesting a potential application of these drugs in association with chemotherapeutic drugs to preserve EC function and to reduce the risk for CVDs in long-term cancer survivors