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FLI-1 驱动的人类疾病中的血管内皮细胞调控。

FLI-1-driven regulation of endothelial cells in human diseases.

机构信息

Cancer Center, The First Hospital of Jilin University, No.1 Xinmin Street, Changchun, 130012, China.

出版信息

J Transl Med. 2024 Aug 6;22(1):740. doi: 10.1186/s12967-024-05546-4.

DOI:10.1186/s12967-024-05546-4
PMID:39107790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11302838/
Abstract

Endothelial cells (ECs) are widely distributed in the human body and play crucial roles in the circulatory and immune systems. ECs dysfunction contributes to the progression of various chronic cardiovascular, renal, and metabolic diseases. As a key transcription factor in ECs, FLI-1 is involved in the differentiation, migration, proliferation, angiogenesis and blood coagulation of ECs. Imbalanced FLI-1 expression in ECs can lead to various diseases. Low FLI-1 expression leads to systemic sclerosis by promoting fibrosis and vascular lesions, to pulmonary arterial hypertension by promoting a local inflammatory state and vascular lesions, and to tumour metastasis by promoting the EndMT process. High FLI-1 expression leads to lupus nephritis by promoting a local inflammatory state. Therefore, FLI-1 in ECs may be a good target for the treatment of the abovementioned diseases. This comprehensive review provides the first overview of FLI-1-mediated regulation of ECs processes, with a focus on its influence on the abovementioned diseases and existing FLI-1-targeted drugs. A better understanding of the role of FLI-1 in ECs may facilitate the design of more effective targeted therapies for clinical applications, particularly for tumour treatment.

摘要

内皮细胞(ECs)广泛分布于人体,在循环和免疫系统中发挥着关键作用。ECs 功能障碍会导致多种慢性心血管、肾脏和代谢疾病的进展。作为 ECs 中的关键转录因子,FLI-1 参与 ECs 的分化、迁移、增殖、血管生成和血液凝固。ECs 中 FLI-1 的表达失衡会导致各种疾病。FLI-1 表达降低会通过促进纤维化和血管损伤导致全身性硬皮病,通过促进局部炎症状态和血管损伤导致肺动脉高压,通过促进 EndMT 过程导致肿瘤转移。FLI-1 表达升高会通过促进局部炎症状态导致狼疮性肾炎。因此,ECs 中的 FLI-1 可能是治疗上述疾病的一个很好的靶点。本综述首次全面概述了 FLI-1 介导的 ECs 过程调节,重点介绍了其对上述疾病和现有 FLI-1 靶向药物的影响。更好地了解 FLI-1 在 ECs 中的作用可能有助于设计更有效的靶向治疗方法,用于临床应用,特别是肿瘤治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/3699d20894c0/12967_2024_5546_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/02008181bfbd/12967_2024_5546_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/3a5aa64ec646/12967_2024_5546_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/fc5da80fe0fb/12967_2024_5546_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/3699d20894c0/12967_2024_5546_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/02008181bfbd/12967_2024_5546_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/3a5aa64ec646/12967_2024_5546_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/fc5da80fe0fb/12967_2024_5546_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/257a/11302838/3699d20894c0/12967_2024_5546_Fig4_HTML.jpg

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