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在性急性损伤中circHIPK3在线粒体功能中的分子机制

Lili Tang^1,2, Jie Zhang^1,2, Jing Han^1,2

¹Department of Critical Care Medicine, The Fifth Affiliated Hospital (Zhuhai) of Zunyi Medical University, Zhuhai, People's Republic of China.

Environmental toxicology

|January 11, 2024

概括

循环RNA HIPK3 (circHIPK3) 通过通过miR-148b-3p/DNMT1/3a/Klotho通路增加糖分和线粒体功能障碍,从而加剧败血性急性损伤 (SAKI),影响细胞衰老.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

败血性急性损伤 (SAKI) 涉及细胞衰老,糖解和线粒体功能障碍.
循环RNAs (circRNAs) 正在成为各种疾病的关键调节者.

研究的目的:

在SAKI期间调查circHIPK3在线粒体功能中的作用.
阐明涉及miR-148b-3p/DNMT1/3a/Klotho轴和线粒体酸盐载体1 (MPC1) 的潜在分子机制.

主要方法:

已建立的SAKI小鼠和人类管状上皮细胞模型.
使用了西方斑点,JC-1染色,流细胞计和各种生物化学分析 (乳酸盐,ATP,OCR,ECAR).
通过功能测试和组织学分析 (H&E,PAS,SA-β-gal染色) 验证了MPC1的作用.

主要成果:

循环HIPK3下调改善了糖解和线粒体功能障碍在体内和体外.
环HIPK3/miR-148b-3p/DNMT1/3a/Klotho轴调节了糖解和线粒体功能.
通过增加乳酸盐和降低ATP和线粒体膜潜能 (MMP),MPC1的敲击加剧了SAKI.

结论:

在SAKI中,circHIPK3促进糖解和线粒体功能障碍.
这种miR-148b-3p/DNMT1/3a/Klotho通路是circHIPK3作用的关键调解者.
circHIPK3通过抑制MPC1在乳酸生产中的调节作用和恶化线粒体功能障碍和衰老来加剧SAKI.

关键词:

这是一种Candida Candida.在MPC1中,MPC1是MPC1.在 circHIPK3K3中使用.线粒体功能线粒体功能败血症急性损伤败血症急性损伤

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