Dysfunction of the renal-vascular axis amplifies VEGFi-induced vascular toxicity, highlighting new biomarkers and targets to mitigate cardiovascular injury in cancer patients.
What is the role of the renal-vascular axis in vascular endothelial growth factor-inhibitor (VEGFi) vascular toxicity in cancer patients?
The renal-vascular axis plays a crucial role in VEGFi-induced vascular toxicity, offering potential novel biomarkers and therapeutic targets to improve cardiovascular safety in cancer patients.
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Abstract Vascular toxicity is a growing concern in cancer patients receiving vascular endothelial growth factor inhibitor (VEGFi) therapy, posing a significant threat to patient prognosis. While the primary mechanism of VEGFi‐induced vascular toxicity is linked to redox‐sensitive reactions that disrupt vascular tone, leading to hypertension and endothelial dysfunction, the role of the renal‐vascular axis remains underexplored. This review seeks to clarify the contribution of the renal‐vascular axis to VEGFi‐related toxicity, focusing on key mechanisms such as endothelial dysfunction, activation of the renin‐angiotensin‐aldosterone system, oxidative stress and disrupted glomerular filtration. The renal‐vascular axis is essential for regulating blood pressure and vascular tone, and its dysfunction may amplify VEGFi‐induced cardiovascular injury. By exploring the interplay between renal and vascular systems in this context, we identify novel cardiovascular biomarkers and therapeutic targets that could help mitigate the vascular toxicity of VEGFi therapy. Understanding these mechanisms is crucial for enhancing the cardiovascular safety of cancer treatments and improving patient outcomes.
Whelan et al. (Mon,) reported a other. Dysfunction of the renal-vascular axis amplifies VEGFi-induced vascular toxicity, highlighting new biomarkers and targets to mitigate cardiovascular injury in cancer patients.