Study on the Mechanisms of Hypertension Induced by VEGFR Inhibitors during Antitumor Therapy
Year: 2025
Type: article
Abstract: 随着医学的进步，在不断更新的抗肿瘤药物尤其是靶向药物和免疫疗法以及更完善的抗肿瘤方案下，癌症患者的生存率不断提高，生存周期延长，与此同时，与之伴随而来的心血管疾病成为其主要死因之一。在众多抗肿瘤药物中，我们发现临床上的常用药物血管内皮生长因子受体抑制剂(VEGFRi)会引起患者血压升高，而这种副作用产生后通常需要调整治疗剂量或停止治疗，从而造成对癌症治疗的负面影响。本课题组前期研究发现微血管稀疏可能是此类药物导致高血压的中心环节。因此本文综述了包括微血管稀疏在内的由VEGFRi治疗癌症中引起血压升高的相关机制以及最新进展，此外，还进一步讨论了细胞一氧化氮(NO)生成减少、平滑肌细胞对NO的反应性降低、收缩刺激物的产生或反应增加、血管壁顺应性和弹性降低以及硫化氢(H2S)的生成减少等机制。With advancements in medical science, cancer survival rates have significantly improved due to the development of novel antineoplastic drugs, particularly targeted therapies and immunotherapies, alongside optimized treatment regimens. However, cardiovascular diseases have concurrently emerged as a leading cause of mortality among cancer survivors. Among various antineoplastic drugs, vascular endothelial growth factor receptor inhibitors (VEGFRi) have been clinically observed to induce hypertension, necessitating dose adjustments or discontinuation of treatment, thereby negatively impacting cancer therapy outcomes. Our previous research identified microvascular rarefaction as a central mechanism underlying VEGFRi-induced hypertension. This review summarizes the mechanisms and recent advancements related to VEGFRi-induced hypertension, including microvascular rarefaction, reduced nitric oxide (NO) synthesis, diminished smooth muscle cell responsiveness to NO, increased production or sensitivity to contractile stimuli, decreased vascular wall compliance and elasticity, and reduced hydrogen sulfide (H₂S) generation.
Source: Advances in Clinical Medicine
Author: 升燚 连
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W4412768501