Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada; Alberta Children's Hospital Research Institute, University of Calgary, Calgary, AB, Canada; Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada.
Airway Inflammation Research Group, Snyder Institute for Chronic Disease, University of Calgary, Calgary, AB, Canada; Alberta Children's Hospital Research Institute, University of Calgary, Calgary, AB, Canada; Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada; Department of Pathology and Laboratory Medicine, University of Calgary, Calgary, AB, Canada.
Chest. 2019 Dec;156(6):1254-1267. doi: 10.1016/j.chest.2019.08.1917. Epub 2019 Aug 28.
Airway remodeling is a characteristic feature of asthma and is thought to play an important role in the pathogenesis of airway hyperresponsiveness. Myofibroblasts are key structural cells involved in injury and repair, and there is evidence that dysregulation of their normal function contributes to airway remodeling. Despite the importance of myofibroblasts, a lack of specific cellular markers and inconsistent nomenclature have limited recognition of their key role in airway remodeling. Myofibroblasts are increased several-fold in the airways in asthma, in proportion to the severity of the disease. Myofibroblasts are postulated to be derived from both tissue-resident and bone marrow-derived cells, depending on the stage of injury and the tissue. A small number of studies have demonstrated attenuation of myofibroblast numbers and also reversal of established myofibroblast populations in asthma and other inflammatory processes. In this article, we review what is currently known about the biology of myofibroblasts in the airways in asthma and identify potential targets to reduce or reverse the remodeling process. However, further translational research is required to better understand the mechanistic role of the myofibroblast in asthma.
气道重塑是哮喘的一个特征性表现，被认为在气道高反应性的发病机制中发挥重要作用。肌成纤维细胞是参与损伤和修复的关键结构细胞，有证据表明其正常功能的失调导致了气道重塑。尽管肌成纤维细胞很重要，但缺乏特异性的细胞标记物和不一致的命名法限制了对其在气道重塑中关键作用的认识。在哮喘的气道中，肌成纤维细胞的数量增加了几倍，与疾病的严重程度成正比。肌成纤维细胞被认为来源于组织固有细胞和骨髓来源细胞，具体取决于损伤的阶段和组织。少数研究表明，在哮喘和其他炎症过程中，肌成纤维细胞数量减少，并且已建立的肌成纤维细胞群体也得到逆转。本文综述了目前已知的哮喘气道中肌成纤维细胞的生物学特性，并确定了减少或逆转重塑过程的潜在靶点。然而，需要进一步的转化研究来更好地理解肌成纤维细胞在哮喘中的机制作用。
