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射血分数保留的心力衰竭:确定活性氧和一氧化氮的作用

Heart failure with preserved ejection fraction: Defining the function of ROS and NO.

作者信息

Zuo Li, Chuang Chia-Chen, Hemmelgarn Benjamin T, Best Thomas M

机构信息

Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio; and

Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio; and.

出版信息

J Appl Physiol (1985). 2015 Oct 15;119(8):944-51. doi: 10.1152/japplphysiol.01149.2014. Epub 2015 May 14.

DOI:10.1152/japplphysiol.01149.2014
PMID:25977452
Abstract

The understanding of complex molecular mechanisms underlying heart failure (HF) is constantly under revision. Recent research has paid much attention to understanding the growing number of patients that exhibit HF symptoms yet have an ejection fraction similar to a normal phenotype. Termed heart failure with preserved ejection fraction (HFpEF), this novel hypothesis traces its roots to a proinflammatory state initiated in part by the existence of comorbidities that create a favorable environment for the production of reactive oxygen species (ROS). Triggering a cascade that involves reduced nitric oxide (NO) availability, elevated ROS levels in the coronary endothelium eventually contribute to hypertrophy and increased resting tension in cardiomyocytes. Improved understanding of the molecular pathways associated with HFpEF has led to studies that concentrate on reducing ROS production in the heart, boosting NO availability, and increasing exercise capacity for HFpEF patients. This review will explore the latest research into the role of ROS and NO in the progression of HFpEF, as well as discuss the encouraging results of numerous therapeutic studies.

摘要

对心力衰竭(HF)潜在复杂分子机制的理解一直在不断修正。最近的研究十分关注越来越多出现HF症状但射血分数与正常表型相似的患者。这种被称为射血分数保留的心力衰竭(HFpEF)的新假说,其根源部分在于由合并症引发的促炎状态,合并症为活性氧(ROS)的产生创造了有利环境。引发一系列涉及一氧化氮(NO)可用性降低的级联反应后,冠状动脉内皮中ROS水平升高最终导致心肌细胞肥大和静息张力增加。对与HFpEF相关分子途径的进一步理解促使了一些研究,这些研究专注于减少心脏中ROS的产生、提高NO可用性以及增加HFpEF患者的运动能力。本综述将探讨ROS和NO在HFpEF进展中作用的最新研究,同时讨论众多治疗研究取得的令人鼓舞的结果。

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