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Methamphetamine exposure increases cardiac microvascular permeability by activating the VEGF-PI3K-Akt-eNOS signaling
Rui Chen1, Peng Huang2, Songren Wei3
1Department of Forensic Medicine, 12453Guangdong Medical University, Dongguan, China.
Abstract:
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.
Insights
Methamphetamine (METH) abuse increases cardiac microvascular permeability by activating the VEGF-PI3K-Akt-eNOS pathway. Bevacizumab treatment effectively reverses these METH-induced effects, offering new therapeutic insights.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Molecular Biology
Background:
- Methamphetamine (METH) is a widely abused psychostimulant.
- METH-induced cardiotoxicity is partly mediated by vascular endothelial growth factor (VEGF).
- The precise mechanisms of METH's impact on cardiac microvascular permeability remain unclear.
Purpose of the Study:
- To investigate the effect of METH on cardiac microvascular permeability.
- To elucidate the role of the VEGF-PI3K-Akt-eNOS signaling pathway in METH-induced effects.
- To evaluate the efficacy of Bevacizumab in mitigating METH-induced cardiac microvascular changes.
Main Methods:
- Exposure of cardiac models to METH.
- Analysis of the VEGF-PI3K-Akt-eNOS signaling pathway activation.
- Assessment of cardiac microvascular permeability.
- Treatment with Bevacizumab to evaluate its therapeutic potential.
Main Results:
- METH exposure significantly enhanced cardiac microvascular permeability.
- METH activated the VEGF-PI3K-Akt-eNOS signaling pathway.
- Bevacizumab treatment effectively reversed the METH-induced increase in cardiac microvascular permeability and pathway activation.
Conclusions:
- METH exposure disrupts cardiac microvascular integrity via the VEGF-PI3K-Akt-eNOS pathway.
- Bevacizumab demonstrates potential as a therapeutic agent against METH-induced cardiac damage.
- This study provides molecular insights into METH cardiotoxicity and suggests a link with Bevacizumab therapy.
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