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首页> 外文期刊>Cardiovascular drugs and therapy >Tmem time: memory T-cells in cardiac allograft vasculopathy : editorial to: 'memory t cells mediate cardiac allograft vasculopathy and are inactivated by anti-OX40L monoclonal antibody' by Hao Wang et al.
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Tmem time: memory T-cells in cardiac allograft vasculopathy : editorial to: 'memory t cells mediate cardiac allograft vasculopathy and are inactivated by anti-OX40L monoclonal antibody' by Hao Wang et al.

机译：Tmem时间：心脏同种异体血管病中的记忆性T细胞：社论：“记忆性t细胞介导心脏同种异体血管病并被抗OX40L单克隆抗体灭活”。

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摘要

Nucleotide metabolism and signalling is directly linked to myocardial function. Therefore analysis how diversity of genes coding nucleotide metabolism related proteins affects clinical progress of heart disease could provide valuable information for development of new treatments. Several studies identified that polymorphism of AMP deaminase 1 gene (AMPD1), in particular the common C34T variant of this gene was found to benefit patients with heart failure and ischemic heart disease. However, these findings were inconsistent in subsequent studies. This prompted our detailed analysis of heart transplant recipients that revealed diverse effect: improved early postoperative cardiac function associated with C34T mutation in donors, but worse 1-year survival. Our other studies on the metabolic impact of AMPD1 C34T mutation revealed decrease in AMPD activity, increased production of adenosine and de-inhibition of AMP regulated protein kinase. Thus, genetic, clinical and biochemical studies revealed that while long term attenuation of AMPD activity could be deleterious, transient inhibition of AMPD activity before acute cardiac injury is protective. We suggest therefore that pharmacological inhibition of AMP deaminase before transient ischemic event such as during ischemic heart disease or cardiac surgery could provide therapeutic benefit.
机译：核苷酸的代谢和信号传导与心肌功能直接相关。因此，分析编码核苷酸代谢相关蛋白的基因多样性如何影响心脏病的临床进展可以为开发新的治疗方法提供有价值的信息。几项研究发现，AMP脱氨酶1基因（AMPD1）的多态性，特别是该基因的常见C34T变体，被发现可以使患有心力衰竭和缺血性心脏病的患者受益。但是，这些发现在随后的研究中并不一致。这促使我们对心脏移植受者进行详细分析，发现其具有多种作用：改善供体中与C34T突变相关的术后早期心脏功能，但1年生存期较差。我们对AMPD1 C34T突变的代谢影响的其他研究表明AMPD活性降低，腺苷产量增加和AMP调节的蛋白激酶去抑制作用。因此，遗传，临床和生化研究表明，虽然AMPD活性的长期降低可能是有害的，但在急性心脏损伤之前暂时抑制AMPD活性是有保护作用的。因此，我们建议在短暂性缺血事件（例如在缺血性心脏病或心脏手术期间）之前对AMP脱氨酶的药理抑制作用可提供治疗益处。

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