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肾纤维化关键细胞及信号通路的研究进展与中药的干预作用

Advances in the study of key cells and signaling pathways in renal fibrosis and the interventional role of Chinese medicines.

作者信息

Liang Lijuan, Mi Youjun, Zhou Shihan, Yang Aojian, Wei Chaoyu, Dai Enlai

机构信息

Gansu University of Chinese Medicine, Lanzhou, China.

Key Laboratory of Dunhuang Medicine and Translation, Ministry of Education, Lanzhou, China.

出版信息

Front Pharmacol. 2024 Dec 2;15:1403227. doi: 10.3389/fphar.2024.1403227. eCollection 2024.

DOI:10.3389/fphar.2024.1403227
PMID:39687302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11647084/
Abstract

Renal fibrosis (RF) is a pathological process characterized by the excessive accumulation of extracellular matrix (ECM), which triggers a repair cascade in response to stimuli and pathogenic factors, leading to the activation of molecular signaling pathways involved in fibrosis. This article discusses the key cells, molecules, and signaling pathways implicated in the pathogenesis of RF, with a particular focus on tubular epithelial cells (TECs), cellular senescence, ferroptosis, autophagy, epithelial-mesenchymal transition (EMT), and transforming growth factor-β(TGF-β)/Smad signaling. These factors drive the core and regulatory pathways that significantly influence RF. A comprehensive understanding of their roles is essential. Through a literature review, we explore recent advancements in traditional Chinese medicine (TCM) aimed at reducing RF and inhibiting chronic kidney disease (CKD). We summarize, analyze, and elaborate on the important role of Chinese herbs in RF, aiming to provide new directions for their application in prevention and treatment, as well as scientific guidance for clinical practices.

摘要

肾纤维化(RF)是一种以细胞外基质(ECM)过度积聚为特征的病理过程,它会触发针对刺激和致病因素的修复级联反应,导致参与纤维化的分子信号通路激活。本文讨论了与RF发病机制相关的关键细胞、分子和信号通路,特别关注肾小管上皮细胞(TECs)、细胞衰老、铁死亡、自噬、上皮-间质转化(EMT)以及转化生长因子-β(TGF-β)/Smad信号传导。这些因素驱动着对RF有显著影响的核心和调节通路。全面了解它们的作用至关重要。通过文献综述,我们探讨了旨在减轻RF和抑制慢性肾脏病(CKD)的传统中医(TCM)的最新进展。我们总结、分析并阐述了中药在RF中的重要作用,旨在为其在预防和治疗中的应用提供新方向,以及为临床实践提供科学指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c2f/11647084/4437fb919c00/fphar-15-1403227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c2f/11647084/72592e860132/fphar-15-1403227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c2f/11647084/4437fb919c00/fphar-15-1403227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c2f/11647084/72592e860132/fphar-15-1403227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c2f/11647084/4437fb919c00/fphar-15-1403227-g002.jpg

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The c-Abl-RACK1-FAK signaling axis promotes renal fibrosis in mice through regulating fibroblast-myofibroblast transition.
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