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TRPV2 channel as a possible drug target for the treatment of heart failure.
Laboratory Investigation ( IF 5.1 ) Pub Date : 2019-12-19 , DOI: 10.1038/s41374-019-0349-z Yuko Iwata 1 , Shin Ito 1 , Shigeo Wakabayashi 2 , Masafumi Kitakaze 1
Laboratory Investigation ( IF 5.1 ) Pub Date : 2019-12-19 , DOI: 10.1038/s41374-019-0349-z Yuko Iwata 1 , Shin Ito 1 , Shigeo Wakabayashi 2 , Masafumi Kitakaze 1
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Heart transplantation is currently the only viable option available for the treatment of severe heart failure conditions such as dilated cardiomyopathy. Hence, novel drugs for treating such conditions need to be developed urgently. Recent studies suggest that Ca2+ overload is involved in the onset and progression of dilated cardiomyopathy, and thus heart failure. The expression and activation of the Ca2+ permeable channel, transient receptor potential vanilloid 2 (TRPV2) channel have been found to play an essential role in sustained intracellular Ca2+ concentration increase, leading to heart failure. However, since there have been no TRPV2-specific inhibitors available until recently, the effect of TRPV2 inhibition on the pathology has not been clearly elucidated. Recent reports show that inhibiting TRPV2 activity effectively improves cardiac function, suppressing myocardial fibrosis and ameliorating the prognosis in animal models of cardiomyopathy with heart failure. In addition to that, inflammation is reported to be involved in the development of heart failure. Here, we review the recent findings on TRPV2 in cardiomyocytes and immune cells involved in the development of heart failure and discuss the current progress of drug development for the treatment of heart failure via targeting TRPV2.
中文翻译：
TRPV2 通道作为治疗心力衰竭的可能药物靶点。
心脏移植目前是治疗扩张型心肌病等严重心力衰竭病症的唯一可行选择。因此，迫切需要开发治疗此类病症的新药。最近的研究表明，Ca2+ 超载与扩张型心肌病以及心力衰竭的发生和发展有关。已发现 Ca2+ 可渗透通道、瞬时受体电位香草素 2 (TRPV2) 通道的表达和激活在持续的细胞内 Ca2+ 浓度增加中发挥重要作用，从而导致心力衰竭。然而，由于直到最近还没有可用的 TRPV2 特异性抑制剂，因此尚未明确阐明 TRPV2 抑制对病理学的影响。最近的报道表明，抑制 TRPV2 活性可有效改善心肌病伴心力衰竭动物模型的心功能，抑制心肌纤维化并改善预后。除此之外，据报道炎症与心力衰竭的发展有关。在此，我们回顾了心肌细胞和免疫细胞中TRPV2与心力衰竭发生发展相关的最新发现，并讨论了靶向TRPV2治疗心力衰竭的药物开发的当前进展。
更新日期：2019-12-20
中文翻译：
TRPV2 通道作为治疗心力衰竭的可能药物靶点。
心脏移植目前是治疗扩张型心肌病等严重心力衰竭病症的唯一可行选择。因此，迫切需要开发治疗此类病症的新药。最近的研究表明，Ca2+ 超载与扩张型心肌病以及心力衰竭的发生和发展有关。已发现 Ca2+ 可渗透通道、瞬时受体电位香草素 2 (TRPV2) 通道的表达和激活在持续的细胞内 Ca2+ 浓度增加中发挥重要作用，从而导致心力衰竭。然而，由于直到最近还没有可用的 TRPV2 特异性抑制剂，因此尚未明确阐明 TRPV2 抑制对病理学的影响。最近的报道表明，抑制 TRPV2 活性可有效改善心肌病伴心力衰竭动物模型的心功能，抑制心肌纤维化并改善预后。除此之外，据报道炎症与心力衰竭的发展有关。在此，我们回顾了心肌细胞和免疫细胞中TRPV2与心力衰竭发生发展相关的最新发现，并讨论了靶向TRPV2治疗心力衰竭的药物开发的当前进展。
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