射血分数保留的心力衰竭分子机制研究进展  

Research progress on the molecular mechanisms of heart failure with preserved ejection fraction

作　　者：周旋 周盛华 张薇 苏慧 ZHOU Xuan;ZHOU Sheng-hua;ZHANG Wei;SU Hui(Department of Geriatrics,First Affiliated Hospital,Air Force Medical University,Xi’an 710032,Shaanxi,China;Department of Pediatrics,First Affiliated Hospital,Air Force Medical University,Xi’an 710032,Shaanxi,China)

机构地区：[1]空军军医大学第一附属医院老年病科,陕西西安710032 [2]空军军医大学第一附属医院儿科,陕西西安710032

出　　处：《心脏杂志》2025年第1期86-93,共8页Chinese Heart Journal

基　　金：陕西省国际科技合作重点项目(2014KW20-01);国家自然科学基金面上项目(31371151);西京医院医务人员培养助推项目(XJZT24LY13)。

摘　　要：射血分数保留的心力衰竭(heart failure with preserved ejection fraction,HFpEF)是一种多表型、高异质性的临床综合征,严重威胁人类健康。其病理生理机制涉及全身多个系统,目前尚未阐明,从而阻碍了基于机制的治疗方法的发展。目前较普遍的观点认为,心血管疾病和其他系统共病导致的全身低度炎症状态通过多种信号通路驱动心脏结构重塑及舒张收缩功能改变,是HFpEF发生的基本范式。HFpEF细胞分子机制复杂,涉及细胞活动的多个方面多个环节。本文重点从NO-cGMP-PKG通路、亚硝化应激、线粒体代谢三个方面对HFpEF分子机制研究进展作一综述,对该病的治疗药物研发具有重要的价值和意义。Heart failure with preserved ejection fraction(HFpEF)is a clinical syndrome with multiple phenotypes and high heterogeneity,which is a serious threat to human health.Its pathophysiology and cellular molecular mechanisms involve multiple systems and have not yet been elucidated,thus impeding the discovery and development of mechanism-based therapies.At present,it is more common to believe that systemic inflammatory states caused by cardiovascular diseases and other systemic comorbidities drive cardiac structural remodeling and diastolic and systolic function changes through multiple signaling pathways,which is the basic paradigm of HFpEF.HFpEF have complex cellularand molecular mechanisms involving multiple aspects and links of cellular activity.This review focuses on the progress of molecular pathological mechanisms of HFpEF from three aspects:NO-cGMP-PKG pathway,oxidative-nitrosative stress and mitochondrial metabolism.It is of great value and significance for the development of therapeutic drugs for this disease.

关 键 词：射血分数保留的心力衰竭 分子机制 NO-cGMP-PKG通路 亚硝化应激 线粒体代谢 

分 类 号：R541.6[医药卫生—心血管疾病]