Abstract
Bronchial asthma is a chronic inflammatory disease in which bronchial wall remodelling plays a significant role. This phenomenon is related to enhanced proliferation of airway smooth muscle cells, elevated extracellular matrix protein secretion and an increased number of myofibroblasts. Phenotypic fibroblast-to-myofibroblast transition represents one of the primary mechanisms by which myofibroblasts arise in fibrotic lung tissue. Fibroblast-to-myofibroblast transition requires a combination of several types of factors, the most important of which are divided into humoural and mechanical factors, as well as certain extracellular matrix proteins. Despite intensive research on the nature of this process, its underlying mechanisms during bronchial airway wall remodelling in asthma are not yet fully clarified. This review focuses on what is known about the nature of fibroblast-to-myofibroblast transition in asthma. We aim to consider possible mechanisms and conditions that may play an important role in fibroblast-to-myofibroblast transition but have not yet been discussed in this context. Recent studies have shown that some inherent and previously undescribed features of fibroblasts can also play a significant role in fibroblast-to-myofibroblast transition. Differences observed between asthmatic and non-asthmatic bronchial fibroblasts (e.g., response to transforming growth factor β, cell shape, elasticity, and protein expression profile) may have a crucial influence on this phenomenon. An accurate understanding and recognition of all factors affecting fibroblast-to-myofibroblast transition might provide an opportunity to discover efficient methods of counteracting this phenomenon.
Highlights
Bronchial asthma is one of the most common chronic diseases in the world
Airway remodelling is defined as a sequence of chronic structural changes that lead to thickening of the airway wall, epithelial damage, subepithelial fibrosis, increased deposition of extracellular matrix (ECM), smooth muscle hypertrophy, and increased vascularity [3–6]
It is well documented that the lungs of patients with asthma are characterized by airway narrowing and increased thickness of the airway wall, which correlate with the severity of bronchial asthma [21, 22]
Summary
Bronchial asthma is one of the most common chronic diseases in the world. It affects over 10% of the human population, and its prevalence is still rising. Airway remodelling is defined as a sequence of chronic structural changes that lead to thickening of the airway wall, epithelial damage, subepithelial fibrosis, increased deposition of extracellular matrix (ECM), smooth muscle hypertrophy, and increased vascularity [3–6]. It is well documented that the lungs of patients with asthma are characterized by airway narrowing and increased thickness of the airway wall (thickening of muscle bundles and subepithelial fibrosis), which correlate with the severity of bronchial asthma [21, 22]. To complete the picture of events occurring in AS bronchial walls, fibroblasts, myofibroblasts and their interactions should be considered These remarkable cells appear to be crucial for the changes leading to narrowing of the airway lumen. We aim to assemble the current knowledge on components and processes that may lead to myofibroblast formation, especially as a result of fibroblastto-myofibroblast transition (FMT) in bronchial asthma
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