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作 者:杨帆[1] 吴建军 YANG Fan;WU Jianjun(Key Laboratory of Myocardial Ischemia,the 2nd Affiliated Hospital of Harbin Medical University,Harbin 150001,China;Department of Cardiology,the 2nd Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
机构地区:[1]哈尔滨医科大学附属第二医院心肌缺血教育部重点实验室,黑龙江省哈尔滨市150001 [2]哈尔滨医科大学附属第二医院心血管内科,黑龙江省哈尔滨市150001
出 处:《实用心脑肺血管病杂志》2021年第9期137-140,共4页Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease
基 金:国家自然科学基金青年科学基金项目(81901853);心肌缺血教育部重点实验室开放课题(KF202010);哈尔滨医科大学创新基金。
摘 要:肺动脉高压(PAH)是一种以肺动脉远端进行性狭窄为特征的复杂疾病,其最终可导致患者右心衰竭甚至死亡。近年研究表明,肺动脉平滑肌细胞(PASMCs)可诱导血管收缩和血管重塑,引起肺血管病理结构异常及肺血管阻力持续升高,进而促进PAH的发生发展。与一氧化氮(NO)和一氧化碳(CO)相似,硫化氢(H2S)可以内源性生成并通过细胞膜扩散,其对心血管系统具有保护作用。笔者通过检索、分析文献发现,H2S调控PASMCs的机制可能为通过血管内皮细胞生长因子(VEGF)/Akt/内皮型一氧化氮合酶(eNOS)途径释放NO,进而扩张血管,或通过CHOP/活化转录因子6(ATF-6)途径减轻内质网应激,还可能通过激活核因子相关因子2(Nrf-2)而影响抗氧化系统,这可能为PAH的治疗提供新的思路。Pulmonary arterial hypertension(PAH)is a complex disease characterized by progressive stenosis of the distal pulmonary artery,which can causes right ventricular failure and death.Recent studies have shown that,pulmonary artery smooth muscle cells(PASMCs)cause abnormal pathological structure of pulmonary vessels and continuous increase of pulmonary vascular resistance,thereby promoting the progress of PAH.Similar to nitric oxide(NO)and carbon monoxide(CO),hydrogen sulfide(H2S)can be produced endogenous and diffused through cell membrane,which has a protective effect on cardiovascular system.By searching and analyzing the literature,the author found that the mechanism of H2S regulating PASMCs may be to release NO through vascular endothelial growth factor(VEGF)/Akt/endothelial nitric oxide synthase(eNOS)pathway and then dilate blood vessels,or reduce endoplasmic reticulum stress through CHOP/activated transcription factor 6(ATF-6)pathway,as well as affect the antioxidant system by activating stimulating nuclear factor erythroid 2-related factor 2(Nrf-2),this may provide a new idea for the treatment of PAH.
关 键 词:肺动脉高压 硫化氢 肺血管平滑肌细胞 血管重塑 综述
分 类 号:R544[医药卫生—心血管疾病]
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