氧化应激在射血分数保留的心力衰竭发病机制与治疗的研究进展

Research progress of oxidative stress in the pathogenesis and treatment of heart failure with preserved ejection fraction

随着对射血分数保留的心力衰竭(HFpEF)发病机制的深入研究,人们发现氧化应激在其发病机制及预后中发挥了重要作用。氧化应激产生的大量活性氧,可诱导线粒体转换孔的开放、转录因子的过表达,从而影响线粒体功能。氧化应激还可通过内质网应激、一氧化氮利用度降低及氧化应激相关分子的过表达等机制,使心肌细胞凋亡增加和心室舒张功能降低。因此,抗氧化应激治疗可能是HFpEF患者的治疗方式之一。

With the increasing study on the mechanism of heart failure with preserved ejection fraction(HFpEF),it has been found that oxidative stress plays a vital role in the pathogenesis and prognosis.The increased concentrations of reactive oxygen species produced by oxidative stress could induce mitochondrial permeability transition pore opening and transcription factors over-expressing.Oxidative stress can induce myocardial apoptosis and diastolic dysfunction through a series of mechanisms,including decreased nitric oxide bioavailability,endoplasmic reticulum stress and increased related cytokines expression.Therefore,the anti-oxidative stress intervention may be an effective therapeutic choice of HFpEF.