Abstract

Asthma is characterized by both chronic inflammation and airway remodeling. Remodeling - the structural changes seen in asthmatic airways - is pivotal in the pathogenesis of the disease. Although significant advances have been made recently in understanding the different aspects of airway remodeling, the exact biology governing these changes remains poorly understood. There is broad agreement that, in asthma, increased airway smooth muscle mass, in part due to smooth muscle hyperplasia, is a very significant component of airway remodeling. However, significant debate persists on the origins of these airway smooth muscle cells. In this review article we will explore the natural history of airway remodeling in asthma and we will discuss the possible contribution of progenitors, stem cells and epithelial cells in mesenchymal cell changes, namely airway smooth muscle hyperplasia seen in the asthmatic airways.

Highlights

  • The immunopathological features of asthma include chronic airway inflammation and airway remodeling [1]

  • A collective term describing the wide range of histopathological structural changes seen in the asthmatic airway wall, has been recognized for almost a century; significant gaps still remain in our understanding of various aspects, including its natural history, etiology, molecular and cellular basis and, more importantly, its clinical and physiological relevance

  • Most of the aforementioned characteristics of airway remodeling contribute to the airway narrowing seen in asthma, increased airway smooth muscle (ASM) mass, due to both ASM hyperplasia and hypertrophy, and sub-epithelial fibrosis, are the most critical

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Summary

Introduction

The immunopathological features of asthma include chronic airway inflammation and airway remodeling [1]. Airway remodeling is characterized by increased airway smooth muscle (ASM) mass, sub-epithelial fibrosis, goblet Most of the aforementioned characteristics of airway remodeling contribute to the airway narrowing seen in asthma, increased ASM mass, due to both ASM hyperplasia and hypertrophy, and sub-epithelial fibrosis, are the most critical.

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