Furthermore, miR-148b-3p can target CDK5R1 and inhibit its expression. The current study indicated that the miR-148b-3p-CDK5R1 axis plays a critical role in apoptosis and mitochondrial dysfunction in stroke.
除此之外，miR-148-3P靶向CDK5R1并抑制它的表达。最近的研究指出，中风时，miR-148-3P-CDK5R1轴在细胞凋亡和线粒体功能障碍中起到重要作用。
CDK5R1 is a coactivator of CDK5, which acts as a major tau kinase and plays a key role in cerebral ischemia. Elevated CDK5 expression can enhance neuronal death in IS, which is consistent with our findings.
CDK5R1是CDK5的激活因子，作为主要的tau 激酶在脑缺血再灌注中起着重要的作用。下调CDK5的表达会增加脑缺血时神经元死亡，这与我们的发现一致。
In this study, we identified a new regulatory mechanism of CDK5R1 expression. To the best of our knowledge, this research is the first to demonstrate that CDK5R1, as a downstream effector of circHIPK3, regulates apoptosis and mitochondrial dysfunction triggered by OGD-R, further supporting our speculation that the circHIPK3-miR-148b-3p-CDK5R1 axis contributes to apoptosis and mitochondrial dysfunction after IS.
在本研究中，我们证实了一种调控CDK5R1表达的新机制。据我们所知，本研究是首次证明CDK5R1，作为circHIPK3的下游基因，调控由缺氧复氧引起的细胞凋亡和线粒体功能障碍，进一步的支持了我们的假设，即脑缺血后circHIPK-miR-148b-3p-CDK5R1轴参与调节细胞凋亡和线粒体功能障碍
The present study also revealed that CDK5R1 downregulated SIRT1 expression to promote OGD-induced BMEC apoptosis and mitochondrial dysfunction. CDK5 expression has been demonstrated to be negatively associated with SIRT1 expression.
现有的研究也揭示了CDK5R1会下调SIRT1的表达去促进缺氧缺糖诱导的BMEC细胞凋亡和线粒体功能障碍。CDK5的表达也已被证实会反向调控SIRT的表达。
As a critical factor implicated in many diseases, including cerebral ischemia, SIRT1 exerts neuroprotective effects, as its activation attenuates cerebral ischemia damage. Upregulation of SIRT1 expression leads to elevation of anti-apoptotic Bcl-2 levels and a decrease in proapoptotic Bax levels, thus suppressing cell death and mitochondrial dysfunction and protecting against cerebral I/R injury. These findings suggest that CDK5R1-mediated downregulation of SIRT1 expression can trigger BMEC apoptosis and mitochondrial dysfunction in a mouse IS model.
作为一个与许多疾病相关的关键因子，SIRT在包括脑缺血的疾病中是起到神经保护作用的，因为它的激活会减轻脑缺血损伤。SIRT1表达的上调会导致抗凋亡分子bcl-2的水平升高，促凋亡分子bax的水平降低，因此抑制细胞死亡和线粒体功能障碍，以抵抗脑缺血再灌注损伤。这些发现都支持，在小鼠脑缺血模型中，CDK5R1调控SIRT1表达下调会引发BMEC凋亡和线粒体功能障碍。
