Kriegel Alison J, Gartz Melanie, Afzal Muhammad Z, de Lange Willem J, Ralphe J Carter, Strande Jennifer L
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.
J Cardiovasc Transl Res. 2017 Jun;10(3):295-304. doi: 10.1007/s12265-016-9723-z. Epub 2016 Dec 28.
Heart failure with preserved left ventricular ejection fraction (HFpEF) has emerged as one of the largest unmet needs in cardiovascular medicine. HFpEF is increasing in prevalence and causes significant morbidity, mortality, and health care resource utilization. Patients have multiple co-morbidities which contribute to the disease complexity. To date, no effective treatment for HFpEF has been identified. The paucity of cardiac biopsies from this patient population and the absence of well-accepted animal models limit our understanding of the underlying molecular mechanisms of HFpEF. In this review, we discuss combining state-of-the-art technologies of microRNA profiling and human induced pluripotent cell-derived cardiomyocytes (iPSC-CMs) in order to uncover novel molecular pathways that may contribute to the development of HFpEF. Here, we focus the advantages and limitations of microRNA profiling and iPSC-CMs as a disease model system to discover molecular mechanisms in HFpEF.
射血分数保留的心力衰竭（HFpEF）已成为心血管医学中最大的未满足需求之一。HFpEF的患病率正在上升，并导致显著的发病率、死亡率和医疗资源利用。患者有多种合并症，这增加了疾病的复杂性。迄今为止，尚未确定针对HFpEF的有效治疗方法。来自该患者群体的心脏活检样本稀少，且缺乏广泛认可的动物模型，这限制了我们对HFpEF潜在分子机制的理解。在本综述中，我们讨论了将微小RNA谱分析和人诱导多能干细胞衍生的心肌细胞（iPSC-CMs）的前沿技术相结合，以揭示可能导致HFpEF发生发展的新分子途径。在此，我们重点探讨微小RNA谱分析和iPSC-CMs作为疾病模型系统在发现HFpEF分子机制方面的优势和局限性。
