Stroke is the second largest cause of death worldwide. Angiotensin converting enzyme (ACE) gene has emerged as an important player in the pathogenesis of hypertension and consequently stroke. It encodes ACE enzyme that converts the inactive decapeptide angiotensin I to active octapeptide, angiotensin II (Ang II). Dysregulation in the expression of ACE gene, on account of genetic variants or regulation by miRNAs, alters the levels of ACE in the circulation. Variable expression of ACE affects the levels of Ang II. Ang II acts through different signal transduction pathways via various tyrosine kinases (receptor/non-receptor) and protein serine/threonine kinases, initiating a downstream cascade of molecular events. In turn these activated molecular pathways might lead to hypertension and inflammation thereby resulting in cardiovascular and cerebrovascular diseases including stroke. In order to regulate the overexpression of ACE, many ACE inhibitors and blockers have been developed, some of which are still under clinical trials.

中文翻译：

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ACE引发的高血压诱发中风：遗传，分子和治疗方面。

中风是全球第二大死亡原因。血管紧张素转换酶（ACE）基因已成为高血压和中风发病的重要因素。它编码ACE酶，可将无活性的十肽血管紧张素I转换为有活性的八肽血管紧张素II（Ang II）。由于遗传变异或miRNA的调控，ACE基因表达失调会改变循环中ACE的水平。ACE的可变表达影响Ang II的水平。Ang II通过各种酪氨酸激酶（受体/非受体）和蛋白丝氨酸/苏氨酸激酶通过不同的信号转导途径起作用，从而引发下游的分子事件级联反应。这些活化的分子途径进而可能导致高血压和炎症，从而导致包括中风在内的心血管和脑血管疾病。为了调节ACE的过表达，已经开发了许多ACE抑制剂和阻滞剂，其中一些仍在临床试验中。