高原肺水肿的分子机制及防治研究进展  

Research Progress in Molecular Mechanism,Prevention and Treatment of High Altitude Pulmonary Edema

作　　者：王梦杰 赵万花 赵鑫杰 唐浩杰 宋丹 WANG Mengjie;ZHAO Wanhua;ZHAO Xinjie;TANG Haojie;SONG Dan(Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region,School of Medicine,Xizang Minzu University,Xianyang 712082,China)

机构地区：[1]西藏民族大学医学院西藏高原相关疾病分子遗传机制与干预研究省级重点实验室,陕西咸阳712082

出　　处：《医学综述》2023年第17期3346-3351,共6页Medical Recapitulate

基　　金：国家自然科学基金(32160165);西藏自治区自然科学基金(XZ202201ZR0065G);西藏民族大学研究生科研创新与实践项目(Y2022098)。

摘　　要：高原肺水肿(HAPE)是影响需要迅速抵达高原人群、国防相关人员等健康状况的主要因素之一。HAPE发病机制较为复杂,其治疗的分子机制尚不清楚,目前治疗仍以吸入一氧化氮舒张肺血管和激素类药物减轻炎症反应为主,但毒副作用强,并不是临床治疗的最佳选择。近年认为,醛糖还原酶(AR)可通过加速肺动脉高压、肺部炎症疾病和渗透性胁迫等病理过程参与HAPE的发生。AR抑制剂可能成为HAPE新的治疗靶点,因此有必要在分子水平阐明其发病机制,这对HAPE的治疗有重要意义。High altitude pulmonary edema(HAPE)is one of the main factors that affect the health status of the people who need to enter the high altitude quickly and the national defense related personnel.The pathogenesis of HAPE is complex.The molecular mechanism of HAPE treatment is not clear,and the current treatment of HAPE is still based on inhaled nitric oxide to relax pulmonary blood vessels and hormonal drugs to reduce inflammation,which have strong toxic side effects,therefore are not the optimal choice for the clinical treatment.Recent reports indicated that aldose reductase(AR)can participated in HAPE through pathological processes such as accelerating the development of pulmonary hypertension,pulmonary inflammatory disease and osmotic stress.AR inhibitors may be a new therapeutic target for HAPE.TTherefore,it is necessary to elucidate the pathogenesis at the molecular level,which will be of great significance for the treatment of HAPE.

关 键 词：高原肺水肿 发病机制 醛糖还原酶 醛糖还原酶抑制剂 

分 类 号：R594.3[医药卫生—内科学]