血管紧张素原再审视:高血压研究中的演变视角
Kanbay, M., Guldan, M., Ozbek, L., Al-Shiab, R., & Laffin, L.J. (2026). Angiotensinogen Reconsidered: Evolving Perspectives in Hypertension Research. Hypertension. https://doi.org/10.1161/HYPERTENSIONAHA.125.26091
Kanbay M, Guldan M, Ozbek L, Al-Shiab R, Laffin LJ. Angiotensinogen Reconsidered: Evolving Perspectives in Hypertension Research. Hypertension. 2026; doi: 10.1161/HYPERTENSIONAHA.125.26091
Kanbay M, Guldan M, Ozbek L, et al. Angiotensinogen Reconsidered: Evolving Perspectives in Hypertension Research[J]. Hypertension. 2026. DOI: 10.1161/HYPERTENSIONAHA.125.26091.
@article{kanbay2026,
author = {Mehmet Kanbay and Mustafa Guldan and Lale Ozbek and Randa Al-Shiab and Linda J Laffin},
title = {Angiotensinogen Reconsidered: Evolving Perspectives in Hypertension Research},
journal = {Hypertension},
year = {2026},
doi = {10.1161/HYPERTENSIONAHA.125.26091},
note = {PMID: 41853854},
}
TY - JOUR AU - Mehmet Kanbay AU - Mustafa Guldan AU - Lale Ozbek AU - Randa Al-Shiab AU - Linda J Laffin TI - Angiotensinogen Reconsidered: Evolving Perspectives in Hypertension Research T2 - Hypertension PY - 2026 DO - 10.1161/HYPERTENSIONAHA.125.26091 AN - PMID:41853854 ER -
高血压是心血管疾病、卒中、慢性肾病和过早死亡的首要可改变危险因素。虽然血管紧张素原是肾素-血管紧张素-醛固酮系统的核心组成部分,但历史上主要将其视为生化底物而非血压的主动调节因子,与血管紧张素转换酶和血管紧张素II受体等下游成分相比,作为治疗靶点的关注度较低。然而,新出现的证据突出了其在血压调节中的动态、组织特异性作用及其对代谢、激素和炎症刺激的应答。本综述检查了血管紧张素原的分子生物学、结构-功能关系和调节机制,包括M235T和-6G>A等遗传变异对个体和群体水平高血压易感性的贡献。进一步探讨了血管紧张素原在盐敏感性高血压、肥胖相关炎症和肾素-血管紧张素-醛固酮系统逃逸现象中的致病作用。最近的转化进展,包括小干扰RNA(zilebesiran)和反义寡核苷酸(tonlamarsen)等RNA疗法在临床试验中显示出有希望的血压降低效果和良好的安全性。血管紧张素原还显示出作为高血压肾病和治疗反应性生物标志物的潜力。