Discussion of the material basis for prevention and treatment of pulmonary fibrosis using naturally medicinal and edible homologous herbs based on the dynamic process of Nrf2, NF-κB and TGF-β in PF
Yan Li , Jia Zheng , Fei Liu , Xianfeng Tan , Huiping Jiang , Yongde Wang
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引用次数: 0
Abstract
Pulmonary fibrosis (PF) is a progressive chronic lung disease with a high incidence and poor prognosis. Despite extensive research into the mechanisms that initiate and drive the progression of pulmonary fibrosis, developing effective treatments remains challenging due to the multiple etiologies, pathogenic links, and signaling pathways involved in PF. Indeed, nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear factor kappa-B (NF-κB), and transforming growth factor-beta (TGF-β) are central players in the pathogenesis of pulmonary fibrosis, and each of these factors influences distinct yet interconnected processes that collectively contribute to disease progression: Nrf2 upregulates antioxidants to mitigate oxidative stress, NF-κB modulates inflammatory responses, and TGF-β promotes fibroblast activation and extracellular matrix (ECM) deposition, leading to fibrosis. Targeting these pathways may offer therapeutic strategies, uncover new insights and provide potential therapeutic targets for PF. Absolutely, the interactions between Nrf2, NF-κB, and TGF-β pathways are complex and can significantly influence the progression of PF, which indicated that targeting a single pathway may show poor efficacy in managing the condition. Moreover, few therapies that effectively intervene in these pathways have been approved. This review focused on the molecular mechanisms of Nrf2, NF-κB, and TGF-β involving in PF and the material basis of the naturally medicinal and edible homologous herbs, which provides a solid foundation for understanding the disease's pathogenesis, and supports the development of therapeutic drugs or treatments for addressing the complex nature of PF.
肺纤维化是一种发病率高、预后差的进行性慢性肺部疾病。尽管对启动和驱动肺纤维化进展的机制进行了广泛的研究,但由于PF涉及多种病因、致病联系和信号通路,开发有效的治疗方法仍然具有挑战性。事实上,核因子红系2相关因子2 (Nrf2)、核因子κ b (NF-κB)和转化生长因子β (TGF-β)在肺纤维化的发病机制中起着核心作用。这些因素中的每一个都影响不同但相互关联的过程,共同促进疾病进展:Nrf2上调抗氧化剂以减轻氧化应激,NF-κB调节炎症反应,TGF-β促进成纤维细胞活化和细胞外基质(ECM)沉积,导致纤维化。靶向这些通路可能为PF提供治疗策略,揭示新的见解,并提供潜在的治疗靶点。当然,Nrf2、NF-κB和TGF-β通路之间的相互作用是复杂的,可以显著影响PF的进展,这表明靶向单一通路可能对PF的治疗效果不佳。此外,很少有有效干预这些途径的治疗方法被批准。本文综述了Nrf2、NF-κB和TGF-β参与PF的分子机制以及天然药用和食用同源草药的物质基础,为了解PF的发病机制提供了坚实的基础,并为解决PF的复杂性开发治疗药物或治疗方法提供了支持。
期刊介绍:
Biomedicine & Pharmacotherapy stands as a multidisciplinary journal, presenting a spectrum of original research reports, reviews, and communications in the realms of clinical and basic medicine, as well as pharmacology. The journal spans various fields, including Cancer, Nutriceutics, Neurodegenerative, Cardiac, and Infectious Diseases.