Keratin 1: A negative regulator of inflammation and potential treatment for pulmonary arterial hypertension.
Keratin 1: A negative regulator of inflammation and potential treatment for pulmonary arterial hypertension.
复制标题
角蛋白 1：炎症的负调节剂和肺动脉高压的潜在治疗方法。
DOI：
10.1111/apha.13594
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Trittmann,JenniferK
中科院分区：
文献类型：
--
作者：
Trittmann,JenniferK
Zhang等人的这项题为“Keratin 1 attenuates hypoxic pulmonary artery hypertension through suppressing pulmonary artery media smooth muscle expansion”的研究发表在最近一期的I Acta Physiologica i. 1导致这项研究的至少有三个关键思想：（a）角蛋白1（Krt 1）被认为是皮肤先天免疫反应的守门人，因为它在局部和全身炎症中起着重要的调节作用，2（B）炎症是肺动脉高压（PAH）发病机制的核心3和（c）角蛋白可以促进源自人类动脉粥样硬化病变的平滑肌细胞凋亡。4因此，作者假设Krt 1调节肺动脉平滑肌细胞（PASMC）的异常生长，这种异常生长发生在指示PAH的血管重塑中。总之，缺氧减少YY 1导致抑制Krt 1转录直接，通过减少Krt 1启动子刺激和间接通过Dnmt 1介导的Krt 1启动子甲基化。角蛋白1通过抑制肺动脉中膜平滑肌扩张减轻缺氧性肺动脉高压。[摘自文章] Acta Physiologica的版权是Wiley-Blackwell的财产，未经版权保持器的明确书面许可，其内容不得复制或通过电子邮件发送到多个网站或发布到列表服务器。但是，用户可以打印、下载或通过电子邮件发送文章供个人使用。这篇摘要可以删节。对副本的准确性不作任何保证。用户应参考原始出版版本的材料的完整摘要。版权适用于所有摘要。
This study by Zhang et al entitled'Keratin 1 attenuates hypoxic pulmonary artery hypertension through suppressing pulmonary artery media smooth muscle expansion'is presented in a recent edition of I Acta Physiologica i. 1 Leading up to this research were at least three key ideas:(a) that keratin 1 (Krt1) is considered the gatekeeper of the skin's innate immune response for its important regulatory role of both local and systemic inflammation, 2 (b) that inflammation is central to the pathogenesis of pulmonary arterial hypertension (PAH) 3 and (c) that keratins can promote apoptosis of smooth muscle cells derived from human atherosclerotic lesions. 4 Therefore, the authors hypothesized that Krt1 regulates abnormal pulmonary arterial smooth muscle cell (PASMC) growth that occurs in vascular remodelling indicative of PAH. In summary, hypoxia decreases YY1 leading to suppressed Krt1 transcription both directly, by decreased Krt1 promoter stimulation and indirectly through Dnmt1-mediated Krt1 promoter methylation. Keratin 1 attenuates hypoxic pulmonary artery hypertension by suppressing pulmonary artery media smooth muscle expansion.[Extracted from the article]Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. Copyright applies to all Abstracts.