Krueger Kathryn J, Rahman Faith K, Shen Qiuhua, Vacek James, Hiebert John B, Pierce Janet D
School of Nursing, University of Kansas Medical Center, Kansas City, KS, USA.
The University of Kansas Health System, Kansas City, KS, USA.
Ann Transl Med. 2021 Oct;9(19):1504. doi: 10.21037/atm-21-2291.
In this review article, we briefly describe the status of treatment options for HFpEF and the role of mitochondrial dysfunction in the pathogenesis of HFpEF as an alternative therapeutic target. We also examine the mechanisms of D-ribose in cellular energy production and discuss the potential disadvantages and benefits of supplemental use of D-ribose in patients with HFpEF.
Heart failure is a major cardiovascular disease that impacts over 6 million Americans and is one of the leading causes for morbidity and mortality. Patients with heart failure often experience shortness of breath and fatigue along with impaired physical capacity, all leading to poor quality of life. As a subtype of heart failure, heart failure with preserved ejection fraction (HFpEF) is characterized with impaired diastolic function. Currently, there are no effective treatments specifically for HFpEF, thus clinicians and researchers are searching for therapies to improve cardiac function. Emerging evidence indicate that mitochondrial dysfunction and impaired cardiac bioenergetics are among the underlying mechanisms for HFpEF. There is increased interest in investigating the use of supplements such as D-ribose to enhance mitochondrial function and improve production of adenosine triphosphate (ATP).
For this narrative review, more than 100 relevant scientific articles were considered from various databases (e.g., PubMed, Web of Science, CINAHL, and Google Scholar) using the keywords "Heart Failure", "HFpEF", "D-ribose", "ATP", "Mitochondria", Bioenergetics", and "Cellular Respiration".
It is essential to find potential targeted therapeutic treatments for HFpEF. Since there is evidence that the HFpEF is related to impaired myocardial bioenergetics, enhancing mitochondrial function could augment cardiac function. Using a supplement such as D-ribose could improve mitochondrial function by increasing ATP and enhancing cardiac performance for patients with HFpEF. There is a recently completed clinical trial with HFpEF patients that indicates D-ribose increases ATP production and improves cardiac ejection fraction.
在这篇综述文章中,我们简要描述射血分数保留的心力衰竭(HFpEF)治疗方案的现状,以及线粒体功能障碍在HFpEF发病机制中作为替代治疗靶点的作用。我们还研究了D-核糖在细胞能量产生中的机制,并讨论了在HFpEF患者中补充使用D-核糖的潜在弊端和益处。
心力衰竭是一种主要的心血管疾病,影响着超过600万美国人,是发病和死亡的主要原因之一。心力衰竭患者常出现呼吸急促、疲劳以及身体能力受损,所有这些都会导致生活质量下降。作为心力衰竭的一种亚型,射血分数保留的心力衰竭(HFpEF)的特征是舒张功能受损。目前,尚无专门针对HFpEF的有效治疗方法,因此临床医生和研究人员正在寻找改善心脏功能的疗法。新出现的证据表明,线粒体功能障碍和心脏生物能量学受损是HFpEF的潜在机制之一。人们对研究使用D-核糖等补充剂来增强线粒体功能和提高三磷酸腺苷(ATP)的产生越来越感兴趣。
对于这篇叙述性综述,我们使用关键词“心力衰竭”、“HFpEF”、“D-核糖”、“ATP”、“线粒体”、“生物能量学”和“细胞呼吸”,从各种数据库(如PubMed、科学网、护理学与健康领域数据库以及谷歌学术)中筛选了100多篇相关科学文章。
找到针对HFpEF的潜在靶向治疗方法至关重要。由于有证据表明HFpEF与心肌生物能量学受损有关,增强线粒体功能可能会改善心脏功能。使用D-核糖等补充剂可以通过增加ATP来改善线粒体功能,并提高HFpEF患者的心脏性能。最近完成的一项针对HFpEF患者的临床试验表明,D-核糖可增加ATP的产生并改善心脏射血分数。