The development of nasal polyps involves early middle meatus mucous remodeling via TGF-β1 mediated PAI-1 reduction

Liu, Yijun; Shu, Longlan; Jiang, Xiaocong; Zhang, Yue; Chen, Qian; Shen, Yang; Yang, Yucheng

doi:10.1016/j.bjorl.2023.01.007

Cited by 2 publications

(2 citation statements)

References 25 publications

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“…The TGFβ1 signaling pathway has been involved in fibrous remodeling phenomena in several type 2 inflammatory diseases, including bronchial asthma [97,98], atopic dermatitis [99], allergic rhinitis [100], nasal polyposis [101], and idiopathic eosinophilic pneumonia [102], all of them sharing common pathophysiological mechanisms with EoE. The inflammatory and fibrotic phenomena described in these organs are similar to those observed in EoE, and despite the differences in intimate molecular mechanisms, it was assumed that the patterns that occur in asthma [50] could be largely extrapolated to EoE [103].…”

Section: Contribution Of Tgf-β1 To Fibrosis In Eoe: Distinct Methods ...mentioning

confidence: 99%

Fibrous Remodeling in Eosinophilic Esophagitis: Clinical Facts and Pathophysiological Uncertainties

Arias-González,

Rodríguez-Alcolado,

Laserna-Mendieta

et al. 2024

IJMS

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Eosinophilic esophagitis (EoE) is a chronic, progressive, type 2 inflammatory disease with increasing global prevalence. An eosinophil-predominant inflammation that permeates the epithelium and deeper esophageal layers characterizes the disease. Several cytokines, mainly derived from inflammatory T-helper 2 (Th2) cells and epithelial cells, are involved in perpetuating inflammatory responses by increasing surface permeability and promoting tissue remodeling characterized by epithelial–mesenchymal transition (EMT) and collagen deposition. This leads to esophageal strictures and narrow caliber esophagi, which are proportional a patient’s age and untreated disease length. Pathophysiological mechanisms leading to EoE have been described in recent years, and transforming growth factor beta (TGF)-beta have been involved in fibrotic phenomena in EoE. However, evidence on the dependence of these phenomena on TGF-beta is scarce and contradictory. This review provides state-of-the art knowledge on intimate mechanisms of esophageal fibrosis in EoE and its clinical consequences.

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Section: Contribution Of Tgf-β1 To Fibrosis In Eoe: Distinct Methods ...mentioning

confidence: 99%

Fibrous Remodeling in Eosinophilic Esophagitis: Clinical Facts and Pathophysiological Uncertainties

Arias-González,

Rodríguez-Alcolado,

Laserna-Mendieta

et al. 2024

IJMS

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“…TGF-β regulates thrombosis by acting as an inducer of plasminogen activator inhibitor 1 (PAI-1) [ 99 ]. At both the transcriptional and protein levels, TGF-β1, PAI-1, and tissue-type plasminogen activators are found to be decreased in both early-stage and mature nasal polyps compared to healthy sinonasal epithelium [ 100 ]. In nasal mucosa-derived fibroblasts of patients with CRSsNP, thromboxane A2 plays a key role in controlling the expression of chemokines CXCL1 and CXCL8, which are found at high levels in the nasal mucosa of patients with CRSsNP.…”

Section: Epithelial Cell–ecm Crosstalkmentioning

confidence: 99%

Unraveling the Role of Epithelial Cells in the Development of Chronic Rhinosinusitis

Ha,

Cho

2023

IJMS

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The pathophysiology of CRS is multifactorial and complex yet needs to be completed. Recent evidence emphasizes the crucial part played by epithelial cells in the development of CRS. The epithelial cells act as physical barriers and play crucial roles in host defense, including initiating and shaping innate and adaptive immune responses. This review aims to present a comprehensive understanding of the significance of nasal epithelial cells in CRS. New research suggests that epithelial dysfunction plays a role in developing CRS through multiple mechanisms. This refers to issues with a weakened barrier function, disrupted mucociliary clearance, and irregular immune responses. When the epithelial barrier is compromised, it can lead to the passage of pathogens and allergens, triggering inflammation in the body. Furthermore, impaired mucociliary clearance can accumulate pathogens and secretions of inflammatory mediators, promoting chronic inflammation. Epithelial cells can release cytokines and chemokines, which attract and activate immune cells. This can result in an imbalanced immune response that continues to cause inflammation. The interaction between nasal epithelial cells and various immune cells leads to the production of cytokines and chemokines, which can either increase or decrease inflammation. By comprehending the role of epithelial cells in CRS, we can enhance our understanding of the disease’s pathogenesis and explore new therapeutics.

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The development of nasal polyps involves early middle meatus mucous remodeling via TGF-β1 mediated PAI-1 reduction

Cited by 2 publications

References 25 publications

Fibrous Remodeling in Eosinophilic Esophagitis: Clinical Facts and Pathophysiological Uncertainties

Fibrous Remodeling in Eosinophilic Esophagitis: Clinical Facts and Pathophysiological Uncertainties

Unraveling the Role of Epithelial Cells in the Development of Chronic Rhinosinusitis

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