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Updated: Sep 10, 2025

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原蛋白可以通过通过KLF4/NF-κB通路减少巨细胞的M1样极化来缓解SA-AKI

Wei Chunling1, Wang Xiaoqian1, Ding Wei1

  • 1Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.

International immunopharmacology
|August 19, 2025
PubMed
概括

构造原蛋白通过KLF4/NF-κB通路降低M1类巨细胞极化,缓解败血症相关的急性损伤 (SA-AKI). 这减少了细胞的炎症,为SA-AKI提供了潜在的治疗策略.

关键词:
在KLF4KLF4巨细胞是一个巨细胞.这就是SA-AKII.构造原生素是一种构造原生素.

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