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TRPM7 通道作为肺动脉高压治疗新靶点的潜力。

Potential of the TRPM7 channel as a novel therapeutic target for pulmonary arterial hypertension.

机构信息

Department of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.

Department of Physiology, School of Medicine, Fukuoka University, 8-19-1 Nanakuma, Jounan-ku, Fukuoka-shi, Fukuoka 814-0180, Japan.

出版信息

J Smooth Muscle Res. 2022;58(0):50-62. doi: 10.1540/jsmr.58.50.

DOI:10.1540/jsmr.58.50
PMID:35944979
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9364263/
Abstract

Pulmonary arterial hypertension (PAH) is an intractable vascular disease characterized by a progressive increase in pulmonary vascular resistance caused by pulmonary vascular remodeling, which ultimately leads to right-sided heart failure. PAH remains incurable, despite the development of PAH-targeted therapeutics centered on pulmonary artery relaxants. It is necessary to identify the target molecules that contribute to pulmonary artery remodeling. Transient receptor potential (TRP) channels have been suggested to modulate pulmonary artery remodeling. Our study focused on the transient receptor potential ion channel subfamily M, member 7, or the TRPM7 channel, which modulates endothelial-to-mesenchymal transition and smooth muscle proliferation in the pulmonary artery. In this review, we summarize the role and expression profile of TRPM7 channels in PAH progression and discuss TRPM7 channels as possible therapeutic targets. In addition, we discuss the therapeutic effect of a Chinese herbal medicine, Ophiocordyceps sinensis (OCS), on PAH progression, which partly involves TRPM7 inhibition.

摘要

肺动脉高压(PAH)是一种难以治愈的血管疾病,其特征是肺血管重构导致肺血管阻力逐渐增加,最终导致右心衰竭。尽管以肺动脉舒张剂为中心的靶向肺动脉治疗药物已经发展起来,但 PAH 仍然无法治愈。有必要确定导致肺动脉重构的靶分子。瞬时受体电位(TRP)通道被认为可以调节肺动脉重构。我们的研究集中在瞬时受体电位离子通道亚家族 M,成员 7,或 TRPM7 通道,该通道调节肺动脉中的内皮到间充质转化和平滑肌增殖。在这篇综述中,我们总结了 TRPM7 通道在 PAH 进展中的作用和表达谱,并讨论了 TRPM7 通道作为可能的治疗靶点。此外,我们还讨论了中药冬虫夏草(OCS)对 PAH 进展的治疗作用,其中部分涉及 TRPM7 抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc3e/9364263/896010ffb4b9/jsmr-58-050-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc3e/9364263/896010ffb4b9/jsmr-58-050-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc3e/9364263/896010ffb4b9/jsmr-58-050-g001.jpg

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The fluid shear stress sensor TRPM7 regulates tumor cell intravasation.流体剪切应力传感器TRPM7调节肿瘤细胞内渗。
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Chronic hypoxia promoted pulmonary arterial smooth muscle cells proliferation through upregulated calcium-sensing receptorcanonical transient receptor potential 1/6 pathway.
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