Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions

IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Cell Biochemistry and Biophysics Pub Date : 2025-02-19 DOI:10.1007/s12013-025-01696-4
Megh Pravin Vithalkar, Shreya Pradhan, K. S. Sandra, H. B. Bharath, Yogendra Nayak
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Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a severe, rapidly advancing disease that drastically diminishes life expectancy. Without treatment, it can progress to lung cancer. The precise etiology of IPF remains unknown, but inflammation and damage to the alveolar epithelium are widely thought to be pivotal in its development. Research has indicated that activating the NLRP3 inflammasome is a crucial mechanism in IPF pathogenesis, as it triggers the release of pro-inflammatory cytokines such as IL-1β, IL-18, and TGF-β. These cytokines contribute to the myofibroblast differentiation and extracellular matrix (ECM) accumulation. Currently, treatment options for IPF are limited. Only two FDA-approved medications, pirfenidone and nintedanib, are available. While these drugs can decelerate disease progression, they come with a range of side effects and do not cure the disease. Additional treatment strategies primarily involve supportive care and therapy. Emerging research has highlighted that numerous flavonoids derived from traditional medicines can inhibit the critical regulators responsible for activating the NLRP3 inflammasome. These flavonoids show promise as potential therapeutic agents for managing IPF, offering a new avenue for treatment that targets the core inflammatory processes of this debilitating condition.

Graphical Abstract

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调节NLRP3炎性小体在特发性肺纤维化中的作用:黄酮类化合物干预的综合综述。
特发性肺纤维化(IPF)是一种严重的、进展迅速的疾病,会大大降低预期寿命。如果不进行治疗,它可能会发展为肺癌。IPF的确切病因尚不清楚,但炎症和肺泡上皮损伤被广泛认为是其发展的关键。研究表明,激活NLRP3炎性小体是IPF发病的重要机制,因为它触发IL-1β、IL-18、TGF-β等促炎细胞因子的释放。这些细胞因子有助于肌成纤维细胞分化和细胞外基质(ECM)的积累。目前,IPF的治疗方案有限。目前只有两种fda批准的药物,吡非尼酮和尼达尼布可用。虽然这些药物可以减缓疾病进展,但它们会带来一系列副作用,而且不能治愈疾病。其他治疗策略主要包括支持性护理和治疗。新兴研究强调,从传统药物中提取的许多类黄酮可以抑制负责激活NLRP3炎症小体的关键调节因子。这些类黄酮有望成为治疗IPF的潜在药物,为治疗这种衰弱性疾病的核心炎症过程提供了新的途径。
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来源期刊
Cell Biochemistry and Biophysics
Cell Biochemistry and Biophysics 生物-生化与分子生物学
CiteScore
4.40
自引率
0.00%
发文量
72
审稿时长
7.5 months
期刊介绍: Cell Biochemistry and Biophysics (CBB) aims to publish papers on the nature of the biochemical and biophysical mechanisms underlying the structure, control and function of cellular systems The reports should be within the framework of modern biochemistry and chemistry, biophysics and cell physiology, physics and engineering, molecular and structural biology. The relationship between molecular structure and function under investigation is emphasized. Examples of subject areas that CBB publishes are: · biochemical and biophysical aspects of cell structure and function; · interactions of cells and their molecular/macromolecular constituents; · innovative developments in genetic and biomolecular engineering; · computer-based analysis of tissues, cells, cell networks, organelles, and molecular/macromolecular assemblies; · photometric, spectroscopic, microscopic, mechanical, and electrical methodologies/techniques in analytical cytology, cytometry and innovative instrument design For articles that focus on computational aspects, authors should be clear about which docking and molecular dynamics algorithms or software packages are being used as well as details on the system parameterization, simulations conditions etc. In addition, docking calculations (virtual screening, QSAR, etc.) should be validated either by experimental studies or one or more reliable theoretical cross-validation methods.
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