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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.