线粒体相关功能障碍在射血分数保留的心力衰竭中的重要作用

Important role of mitochondria-related dysfunction in heart failure with preserved ejection fraction

射血分数保留的心力衰竭(HFpEF)现已成为心力衰竭的主要类型,其临床症状具有高度异质性,预后较差,且发病率仍在不断增长。受多种危险因素影响,HFpEF的发病机制复杂,病理生理学机制尚未得到阐明,目前仍缺少有效的治疗手段。近年来,学者们发现线粒体功能障碍是多种疾病发生、发展的潜在影响因素。随着研究不断深入,线粒体功能障碍在HFpEF发生发展中的重要作用开始得到认可,靶向线粒体功能障碍有可能成为制订HFpEF治疗策略的突破点之一。本文综述线粒体能量代谢、产生活性氧簇、线粒体自噬、调节钙稳态等相关功能在HFpEF病理过程中的研究进展,简述HFpEF的治疗现况,为寻找药物治疗新靶点、减轻HFpEF的临床症状提供新思路。

Heart failure with preserved ejection fraction(HFpEF),which is now the dominant type of heart failure with highly heterogeneous clinical symptoms,poor prognosis,and growing incidence.Affected by a variety of risk factors,the pathogenesis of HFpEF is complex,the pathophysiological mechanism has not been clarified,and there is still a lack of effective treatment.In recent years,researchers have found that mitochondrial dysfunction is a potential factor in the occurrence,and development of many diseases.With the deepening of research,the important role of mitochondrial dysfunction in the occurrence and development of HFpEF is beginning to be recognized,and targeting mitochondrial dysfunction may become one of the breakthrough points in the development of treatment strategies for HFpEF.This paper reviews the research progress of mitochondrial energy metabolism,generation of reactive oxygen species,mitochondrial autophagy,regulation of calcium homeostasis,and other related functions in the pathological process of HFpEF,and briefly describes the current status of treatment of HFpEF,providing new ideas for finding new drug treatment targets and alleviating clinical symptoms of HFpEF.