Methamphetamine (METH) is an illicit amphetamine-like psychostimulant that is commonly abused. However, the modulation of METH-induced cardiac microvascular permeability is still not completely known. Previously, we discovered that the vascular endothelial growth factor (VEGF) regulated the cardiotoxicity produced by METH. In this work, we looked into the effect of METH exposure on cardiac microvascular permeability via the VEGF-PI3K-Akt-eNOS signaling pathway, as well as the efficacy of Bevacizumab treatment in reducing this effect. The findings revealed that METH exposure enhanced cardiac microvascular permeability while also activating the VEGF-PI3K-Akt-eNOS signaling pathway. Furthermore, treatment with Bevacizumab has been shown to be effective in reversing the METH-induced phenomena. Briefly stated, our research may provide fresh insight into the molecular underpinnings of METH-induced cardiac microvascular permeability, and it may also provide evidence for a relationship between METH misuse and Bevacizumab medication.
Keywords: Bevacizumab; Methamphetamine; VEGF-PI3K-Akt-eNOS; cardiac microvascular permeability; vascular hyperpermeability.