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肺特异性互白素6介导的转谷氨酶2激活和心肺纤维化

Krishna C Penumatsa¹, Yamini Sharma¹, Rod R Warburton¹

¹Pulmonary, Critical Care and Sleep Division, Department of Medicine, Tufts Medical Center, Boston, MA, United States.

Frontiers in immunology

|April 23, 2024

概括

介质素6 (IL6) 通过激活转谷氨酶2 (TG2) 和促进组织纤维化来驱动肺高血压 (PH). 这一过程由糖溶性酶pyruvate kinase M2 (PKM2) 调节.

科学领域:

心血管科学心血管科学
肺部医学肺部医学
分子生物学分子生物学

背景情况:

肺高血压 (PH) 涉及炎症和代谢变化,包括改变的葡萄糖分解.
介质蛋白6 (IL6) 和转胺酶2 (TG2) 涉及到心血管疾病,但TG2在PH中的作用尚不清楚.

研究的目的:

为了研究IL6和TG2在肺高血压中介导组织重塑中的分子相互作用.
确定糖溶性重编程在IL6诱导的TG2激活和纤维化中的作用.

主要方法:

使用肺部特定的IL6过度表达的转基因小鼠模型.
评估了右心室缩压,组织重量和肺和RV中的纤维化.
在体内和培养的肺纤维细胞中测量了糖分和纤维素标记物 (HIF-1α,PKM2,TG2).
研究了PKM2的药理抑制对IL6诱导的TG2活性和纤维生成的影响.

主要成果:

过度表达IL6导致RV缩压升高,肺和RV组织重量增加,纤维化增强.
IL6诱导了糖质 (HIF-1α,PKM2) 和纤维素 (TG2) 标记物的表达.
IL6刺激了TG2激活和肺纤维细胞中的细胞外基质积累.
抑制PKM2显著降低了IL6诱导的TG2活性和纤维化.

结论:

通过TG2激活,IL6促进了PH中的心肺重塑和组织纤维化.
糖溶性酶PKM2在IL6诱导的TG2活性和随后的纤维化中起着调节作用.
向PKM2可能为IL6-介导PH和相关组织重塑提供治疗策略.

关键词:

在PKM2中,PKM2是PKM2.纤维化纤维化介质蛋白 6 介质蛋白 6 介质蛋白肺肺肺肺肺肺肺肺肺肺动脉高血压肺动脉高血压右心室的右心室.转谷氨酸酶2的使用

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