Gibb Andrew A, Murray Emma K, Eaton Deborah M, Huynh Anh T, Tomar Dhanendra, Garbincius Joanne F, Kolmetzky Devin W, Berretta Remus M, Wallner Markus, Houser Steven R, Elrod John W
Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA.
Cardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA.
JACC Basic Transl Sci. 2021 Aug 23;6(8):650-672. doi: 10.1016/j.jacbts.2021.07.004. eCollection 2021 Aug.
In this study the authors used systems biology to define progressive changes in metabolism and transcription in a large animal model of heart failure with preserved ejection fraction (HFpEF). Transcriptomic analysis of cardiac tissue, 1-month post-banding, revealed loss of electron transport chain components, and this was supported by changes in metabolism and mitochondrial function, altogether signifying alterations in oxidative metabolism. Established HFpEF, 4 months post-banding, resulted in changes in intermediary metabolism with normalized mitochondrial function. Mitochondrial dysfunction and energetic deficiencies were noted in skeletal muscle at early and late phases of disease, suggesting cardiac-derived signaling contributes to peripheral tissue maladaptation in HFpEF. Collectively, these results provide insights into the cellular biology underlying HFpEF progression.
在本研究中,作者运用系统生物学方法,确定射血分数保留的心力衰竭(HFpEF)大型动物模型中代谢和转录的渐进性变化。在结扎后1个月对心脏组织进行转录组分析,结果显示电子传递链成分缺失,代谢和线粒体功能的变化也证实了这一点,这一切均表明氧化代谢发生了改变。结扎后4个月,已确诊的HFpEF导致中间代谢发生变化,线粒体功能恢复正常。在疾病的早期和晚期,骨骼肌均出现线粒体功能障碍和能量缺乏,提示心脏来源的信号传导导致HFpEF外周组织适应不良。总体而言,这些结果为HFpEF进展的细胞生物学机制提供了见解。