[Advances in pathogenesis of asthma airway remodeling and intervention mechanism of traditional Chinese medicine].

Q3 Pharmacology, Toxicology and Pharmaceutics
Ya-Sheng Deng, Jiang Lin, Yu-Jiang Xi, Yan-Ping Fan, Wen-Yue Li, Yong-Hui Liu, Zhao-Bing Ni, Xi Ming
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Abstract

Asthma, a chronic inflammatory airway disease with a high global prevalence, has a complex pathogenesis, in which airway remodeling plays a key role in the chronicity of the disease. Airway remodeling involves a series of pathophysiological changes, including airway epithelial damage, proliferation of mucous glands and goblet cells, subepithelial fibrosis, proliferation and migration of airway smooth muscle cells, and epithelial-mesenchymal transition. These complex pathological changes significantly increase airway resistance and responsiveness, forming an important pathological basis for refractory asthma. Currently, the regulatory mechanisms of airway remodeling focus on signaling pathways and regulatory targets. The signaling pathways include phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt), nuclear factor-κB(NF-κB), transforming growth factor-β1(TGF-β1)/Smads, and mitogen-activated protein kinase(MAPK). The regulatory targets include microRNAs(miRNAs), competing endogenous RNAs(ceRNAs), long non-coding RNAs(lncRNAs), and circular RNAs(circRNAs). Key proteins involved in these processes include TGF-β1, silencing information regulator 2-related enzyme 1(SIRT1), chitinase 3-like protein 1(YKL-40), and adenosine deaminase-metalloproteinase 33(ADAM33). In recent years, the potential of traditional Chinese medicine in the treatment of asthma has become increasingly evident. Its active ingredients, extracts, and complexes can inhibit airway remodeling in asthma through multiple pathways, demonstrating a variety of effects, including anti-inflammatory actions, inhibition of smooth muscle cell proliferation and migration, regulation of epithelial-mesenchymal transition, attenuation of fibrosis and basement membrane thickening, reduction of mucus secretion, inhibition of vascular remodeling, modulation of immune imbalance, and antioxidative stress. This paper aims to provide an in-depth analysis of the pathogenesis and therapeutic targets of asthma, offering theoretical support and innovative strategies for clinical research and drug development in the treatment of asthma.

[哮喘气道重塑的发病机制及中医干预机制研究进展]。
哮喘是一种全球高发的慢性炎性气道疾病,其发病机制复杂,气道重塑在其慢性性中起关键作用。气道重塑涉及气道上皮损伤、粘膜腺和杯状细胞增生、上皮下纤维化、气道平滑肌细胞增殖迁移、上皮间质转化等一系列病理生理变化。这些复杂的病理变化显著增加气道阻力和反应性,形成难治性哮喘的重要病理基础。目前,气道重塑的调控机制主要集中在信号通路和调控靶点上。信号通路包括磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)、核因子-κB(NF-κB)、转化生长因子-β1(TGF-β1)/Smads、丝裂原活化蛋白激酶(MAPK)。调控靶点包括microRNAs(miRNAs)、竞争内源性rna (ceRNAs)、长链非编码rna (lncRNAs)和环状rna (circRNAs)。参与这些过程的关键蛋白包括TGF-β1、沉默信息调控因子2相关酶1(SIRT1)、几丁质酶3样蛋白1(YKL-40)和腺苷脱氨酶-金属蛋白酶33(ADAM33)。近年来,中医药在治疗哮喘方面的潜力越来越明显。其有效成分、提取物和复合物可通过多种途径抑制哮喘气道重构,表现出多种作用,包括抗炎作用、抑制平滑肌细胞增殖和迁移、调节上皮-间质转化、减弱纤维化和基底膜增厚、减少粘液分泌、抑制血管重构、调节免疫失衡和抗氧化应激。本文旨在深入分析哮喘的发病机制和治疗靶点,为哮喘治疗的临床研究和药物开发提供理论支持和创新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Zhongguo Zhongyao Zazhi
Zhongguo Zhongyao Zazhi Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)
CiteScore
1.50
自引率
0.00%
发文量
581
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