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CXCR4通过改变糖分解来调节巨细胞M1的两极分化,从而促进前列腺纤维化

Yi Zhang^1,2,3, Chen Zhang^1,2,3, Rui Feng⁴

¹Department of Urology, the First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People's Republic of China.

Cell communication and signaling : CCS

|September 26, 2024

概括

阻断C-X-C受体4 (CXCR4) 会减少M1巨分化和前列腺纤维化炎症中的炎症. 这种抑制会影响糖解,并促进转移到M2巨细胞,缓解纤维化发育.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
病理生理学病理生理学

背景情况:

C-X-C受体4 (CXCR4) 是一种保守的G蛋白结合受体,参与人类病理生理过程,包括纤维化.
在前列腺炎纤维化期间,CXCR4在调节巨细胞相关炎症方面的特定作用尚不清楚.

研究的目的:

为了研究CXCR4在调节巨细胞M1极化中的作用,通过在前列腺炎纤维化中的糖解.
在这种情况下,阐明连接CXCR4,糖解和巨两极分化的基础分子机制.

主要方法:

使用可诱导的实验性慢性前列腺炎模型用于前列腺纤维化.
使用lentivirus的巨细胞减少CXCR4表达,并通过腺病毒介导的CXCR4激动剂评估体内效应.
研究了PI3K/AKT/mTOR路径和c-MYC/PFKFB3轴与CXCR4静音相关的情况.

主要成果:

减少CXCR4的表达缓解了在LPS治疗期间M1巨细胞的两极分化.
抑制CXCR4抑制了甘油性新陈代谢,增强了线粒体功能,并促进了M1到M2巨细胞的过渡.
在实验性自身免疫性前列腺炎 (EAP) 中阻断CXCR4可减少炎症和前列腺纤维化发展.

结论:

在前列腺炎纤维化中,CXCR4在促进M1两极化和甘油性新陈代谢方面发挥着至关重要的作用.
沉默CXCR4会削弱PI3K/AKT/mTOR通路,降低c-MYC,然后降低PFKFB3,从而影响巨细胞的两极化和新陈代谢.
向CXCR4通过调节巨细胞极化和炎症反应,为前列腺炎纤维化提供了潜在的治疗策略.

关键词:

慢性前列腺炎慢性前列腺炎纤维化纤维化纤维化葡萄糖溶解是什么? 葡萄糖溶解 M1 M1 的意思是巨细胞是一个巨细胞.

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