首页> 美国卫生研究院文献>BMC Pharmacology Toxicology >Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB
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Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB

机译:心脏血栓素A2受体激活不会直接诱导心肌肥大但会引起庆大霉素和2-APB阻止的细胞死亡

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摘要

BackgroundWe have previously shown that the thromboxane (TXA2) receptor agonist, U46619, can directly induce ventricular arrhythmias that were associated with increases in intracellular calcium in cardiomyocytes. Since TXA2 is an inflammatory mediator and induces direct calcium changes in cardiomyocytes, we hypothesized that TXA2 released during ischemia or inflammation could also cause cardiac remodeling.
机译:背景我们以前已经证明血栓烷(TXA2)受体激动剂U46619可以直接诱发与心肌细胞内钙离子升高有关的室性心律失常。由于TXA2是一种炎症介质,可直接引起心肌细胞钙的变化,因此我们假设缺血或炎症过程中释放的TXA2也可能导致心脏重塑。

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