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对TRPM8通道的遗传删除恢复了微血管功能,并减轻了慢性病的进展

Jenq-Wen Huang¹, Chia-Hui Chen², Ming-Tsun Tsai³

¹Department of Internal Medicine, National Taiwan University Hospital, 7, Chungshan South Road, Zhongzheng District, Taipei, 100225, Taiwan; Department of Internal Medicine, College of Medicine, National Taiwan University, 1, Sec. 1, Jenai Road, Zhongzheng District, Taipei, 100233, Taiwan.

Free radical biology & medicine

|October 10, 2025

概括

过渡性受体潜在拉斯8 (TRPM8) 通道对于慢性病 (CKD) 的进展至关重要. 在小鼠中阻断TRPM8减少了损伤,纤维化和炎症,这表明它是CKD的潜在治疗标.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

慢性病 (CKD) 涉及炎症和纤维化,导致功能下降.
结核病的确切病原机制尚未完全理解.
暂时受体潜能拉斯8 (TRPM8) 通道调节炎症,但它们在CKD中的作用尚不清楚.

研究的目的:

为了研究TRPM8在慢性病的发病过程中的作用.
探索TRPM8作为CKD的潜在治疗点.

主要方法:

来自CKD患者和野生型 (WT) 和TRPM8淘汰赛 (TRPM8-/-) 鼠标的脏样本的分析.
在体外研究中,使用用TNF-α和氧硫酸 (IS) 治疗的内皮细胞 (EC).
评估功能标志物,纤维化,炎症,自和EC完整性的评估.

主要成果:

在CKD患者中,TRPM8mRNA水平与疾病严重程度,纤维化和自基因表达相关.
在小鼠中TRPM8缺失减少了血液尿素,肌,纤维化和炎症.
TRPM8淘汰赛改善了EC完整性,自流和抗氧化能力,并在体外预防了IS/TNF-α诱导的EC功能障碍.

结论:

TRPM8在慢性病的发展和进展中起着重要作用.
对TRPM8的遗传破坏通过增强EC功能和减少炎症来改善损伤.
抑制TRPM8是一种有前途的治疗策略,用于治疗CKD.

关键词:

慢性脏疾病慢性脏疾病内皮质的完整性内皮质的完整性纤维化纤维化纤维化炎症反应是一种炎症反应.暂时的受体潜力 melastatin成员 8 暂时的受体潜力

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