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已发表论文
miR-206 在中性粒细胞哮喘炎症中通过调控 KLF4 影响 Th17 细胞分化的机制
Authors Feng L , Li Y, Zhang L , Xing Y, Huo R, Cheng E, Tian X
Received 1 May 2025
Accepted for publication 22 October 2025
Published 4 November 2025 Volume 2025:18 Pages 1493—1504
DOI https://doi.org/10.2147/JAA.S537623
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Luis Garcia-Marcos
Liting Feng, Yingna Li, Lulu Zhang, Yanqing Xing, Rujie Huo, Erjing Cheng, Xinrui Tian
Department of Gerontology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China
Correspondence: Xinrui Tian, Department of Gerontology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China, Tel +8613834575570, Email tianxr@126.com
Purpose: This study explores the role of miR-206 and KLF4 in neutrophilic asthma, focusing on their interaction and the molecular mechanisms by which miR-206 regulates Th17 cell-mediated immune-inflammatory responses through KLF4.
Methods: RT-qPCR and flow cytometry assessed miR-206, KLF4 mRNA, and Th17 cell levels in asthma patients and healthy controls. CD4+ T cells were transfected to overexpress or inhibit miR-206, and KLF4, IL-17, and Th17 cell ratios were analyzed using RT-qPCR, ELISA, and flow cytometry. Correlation analysis evaluated relationships between miR-206, KLF4, and Th17 cells.
Results: Severe asthma patients showed reduced miR-206 and elevated KLF4 mRNA levels, with increased Th17 cells and IL-17. miR-206 downregulated KLF4, negatively correlating with KLF4, Th17 cells, and IL-17. KLF4 positively correlated with Th17 cells and IL-17. miR-206 suppressed Th17 differentiation and IL-17 production by modulating KLF4.
Conclusion: miR-206 is downregulated in acute asthma and targets KLF4, inhibiting Th17 cell differentiation and IL-17 production. These findings highlight miR-206 as a potential therapeutic target for asthma through its anti-inflammatory effects mediated by KLF4 and Th17 regulation.
Keywords: asthma, miR-206, KLF4, Th17, IL-17
Department of Gerontology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China
Correspondence: Xinrui Tian, Department of Gerontology, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China, Tel +8613834575570, Email tianxr@126.com
Purpose: This study explores the role of miR-206 and KLF4 in neutrophilic asthma, focusing on their interaction and the molecular mechanisms by which miR-206 regulates Th17 cell-mediated immune-inflammatory responses through KLF4.
Methods: RT-qPCR and flow cytometry assessed miR-206, KLF4 mRNA, and Th17 cell levels in asthma patients and healthy controls. CD4+ T cells were transfected to overexpress or inhibit miR-206, and KLF4, IL-17, and Th17 cell ratios were analyzed using RT-qPCR, ELISA, and flow cytometry. Correlation analysis evaluated relationships between miR-206, KLF4, and Th17 cells.
Results: Severe asthma patients showed reduced miR-206 and elevated KLF4 mRNA levels, with increased Th17 cells and IL-17. miR-206 downregulated KLF4, negatively correlating with KLF4, Th17 cells, and IL-17. KLF4 positively correlated with Th17 cells and IL-17. miR-206 suppressed Th17 differentiation and IL-17 production by modulating KLF4.
Conclusion: miR-206 is downregulated in acute asthma and targets KLF4, inhibiting Th17 cell differentiation and IL-17 production. These findings highlight miR-206 as a potential therapeutic target for asthma through its anti-inflammatory effects mediated by KLF4 and Th17 regulation.
Keywords: asthma, miR-206, KLF4, Th17, IL-17