Emerging Novel Therapies for Heart Failure.
Emerging Novel Therapies for Heart Failure.
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DOI：
10.4137/cmc.s29735
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Li JC
中科院分区：
文献类型：
--
作者：
Szema AM;Dang S;Li JC
心脏功能衰竭，当器官不能泵血的速度成比例的身体对氧气的需要，或当这一功能导致心腔充盈压力升高（心源性肺水肿）。尽管我们对心力衰竭有着复杂的知识，但即使是所谓的射血分数保留的心力衰竭也有很高的死亡率和发病率。因此，迫切需要新的治疗方法。本综述讨论了目前心力衰竭的标准治疗方法，并在最近批准的沙库巴曲和伊夫拉定之后，对新兴的新型治疗方法进行了探索。例如，血管活性肠肽（VIP）保护心脏，因此在缺乏VIP的情况下，VIP敲除小鼠在关键心力衰竭基因中具有失调：1）力产生和传播; 2）能量产生和调节; 3）Ca+2循环; 4）转录调节因子。VIP给药导致人类受试者的冠状动脉扩张。在心力衰竭患者中，VIP水平升高是一种合理的内源性保护作用。随着弹性蛋白聚合物的发展，以稳定VIP和防止其降解，VIP可能因此有机会满足未满足的需求，作为一种潜在的治疗急性心力衰竭。
Heart function fails when the organ is unable to pump blood at a rate proportional to the body’s need for oxygen or when this function leads to elevated cardiac chamber filling pressures (cardiogenic pulmonary edema). Despite our sophisticated knowledge of heart failure, even so-called ejection fraction-preserved heart failure has high rates of mortality and morbidity. So, novel therapies are sorely needed. This review discusses current standard therapies for heart failure and launches an exploration into emerging novel treatments on the heels of recently-approved sacubitril and ivbradine. For example, Vasoactive Intestinal Peptide (VIP) is protective of the heart, so in the absence of VIP, VIP knockout mice have dysregulation in key heart failure genes: 1) Force Generation and Propagation; 2) Energy Production and Regulation; 3) Ca+2 Cycling; 4) Transcriptional Regulators. VIP administration leads to coronary dilation in human subjects. In heart failure patients, VIP levels are elevated as a plausible endogenous protective effect. With the development of elastin polymers to stabilize VIP and prevent its degradation, VIP may therefore have a chance to satisfy the unmet need as a potential treatment for acute heart failure.