» Articles » PMID: 30979017

Extracellular Matrix Component Remodeling in Respiratory Diseases: What Has Been Found in Clinical and Experimental Studies?

Overview
Journal Cells
Publisher MDPI
Date 2019 Apr 14
PMID 30979017
Citations 72
Authors
Affiliations
Soon will be listed here.
Abstract

Changes in extracellular matrix (ECM) components in the lungs are associated with the progression of respiratory diseases, such as asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS). Experimental and clinical studies have revealed that structural changes in ECM components occur under chronic inflammatory conditions, and these changes are associated with impaired lung function. In bronchial asthma, elastic and collagen fiber remodeling, mostly in the airway walls, is associated with an increase in mucus secretion, leading to airway hyperreactivity. In COPD, changes in collagen subtypes I and III and elastin, interfere with the mechanical properties of the lungs, and are believed to play a pivotal role in decreased lung elasticity, during emphysema progression. In ARDS, interstitial edema is often accompanied by excessive deposition of fibronectin and collagen subtypes I and III, which can lead to respiratory failure in the intensive care unit. This review uses experimental models and human studies to describe how inflammatory conditions and ECM remodeling contribute to the loss of lung function in these respiratory diseases.

Citing Articles

Collagen deposition in lung parenchyma driven by depletion of interstitial Lyve-1 macrophages prevents cigarette smoke-induced emphysema and loss of airway function.

Dagnachew Y, Lim H, Wupeng L, Lim S, Lim S, Thiam C Front Immunol. 2025; 15():1493395.

PMID: 39830508 PMC: 11738928. DOI: 10.3389/fimmu.2024.1493395.


Targeting cytoskeletal biomechanics to modulate airway smooth muscle contraction in asthma.

McCullough M, Joshi I, Pereira N, Fuentes N, Krishnan R, Druey K J Biol Chem. 2024; 301(1):108028.

PMID: 39615690 PMC: 11721269. DOI: 10.1016/j.jbc.2024.108028.


PDGFRα-positive cell-derived TIMP-1 modulates adaptive immune responses to influenza A viral infection.

Dutta S, Zhu Y, Almuntashiri S, Peh H, Zuniga J, Zhang D Am J Physiol Lung Cell Mol Physiol. 2024; 328(1):L60-L74.

PMID: 39585242 PMC: 11905806. DOI: 10.1152/ajplung.00104.2024.


Gut microbiome and metabolomics in systemic sclerosis: feature, link and mechanisms.

Yao Q, Tan W, Bai F Front Immunol. 2024; 15:1475528.

PMID: 39559369 PMC: 11570262. DOI: 10.3389/fimmu.2024.1475528.


The Role of the Extracellular Matrix in the Pathogenesis and Treatment of Pulmonary Emphysema.

Cantor J Int J Mol Sci. 2024; 25(19).

PMID: 39408941 PMC: 11477147. DOI: 10.3390/ijms251910613.


References
1.
Vasconcelos L, Silva M, Costa A, de Oliveira G, Souza I, Queiroga F . A Guinea Pig Model of Airway Smooth Muscle Hyperreactivity Induced by Chronic Allergic Lung Inflammation: Contribution of Epithelium and Oxidative Stress. Front Pharmacol. 2019; 9:1547. PMC: 6353839. DOI: 10.3389/fphar.2018.01547. View

2.
Tomashefski Jr J . Pulmonary pathology of acute respiratory distress syndrome. Clin Chest Med. 2000; 21(3):435-66. DOI: 10.1016/s0272-5231(05)70158-1. View

3.
Koenders M, Wismans R, Starcher B, Hamel B, Dekhuijzen R, van Kuppevelt T . Fibrillin-1 staining anomalies are associated with increased staining for TGF-beta and elastic fibre degradation; new clues to the pathogenesis of emphysema. J Pathol. 2009; 218(4):446-57. DOI: 10.1002/path.2548. View

4.
TYRRELL D, Horne A, Holme K, Preuss J, Page C . Heparin in inflammation: potential therapeutic applications beyond anticoagulation. Adv Pharmacol. 1999; 46:151-208. DOI: 10.1016/s1054-3589(08)60471-8. View

5.
Lazaar A, Panettieri Jr R . Is airway remodeling clinically relevant in asthma?. Am J Med. 2003; 115(8):652-9. DOI: 10.1016/j.amjmed.2003.07.010. View