Paediatric asthma is a chronic inflammatory airway disease that can cause airway swelling, excessive mucus secretion, and increased smooth muscle tone, leading to airway narrowing and respiratory distress. Airway remodelling involves a series of pathophysiological alterations, including airway epithelial injury, proliferation of mucous glands and goblet cells, subepithelial fibrosis, proliferation and migration of airway smooth muscle cells, and airway epithelial-mesenchymal transition. These complex processes significantly increase airway resistance and reactivity, forming a crucial pathological basis for refractory asthma. With advances in molecular biology, non-coding RNAs such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) have garnered extensive attention due to their pivotal roles in gene expression regulation. Extracellular vesicles (EVs), as membrane-bound particles released by cells, can carry various bioactive molecules including non-coding RNAs, playing a crucial role in intercellular communication and influencing the functional state of recipient cells. In diseases such as asthma, non-coding RNAs participate in regulating processes including airway remodelling, emerging as potential diagnostic biomarkers and therapeutic targets. This narrative review summarises current evidence on EV-associated non-coding RNAs in paediatric asthma airway remodelling, noting that most cited studies used operational EV terminology rather than biogenesis-specific “exosomes” because endosomal origin was not experimentally validated in most cases. Current mechanistic evidence is strongest for miRNA-related studies, whereas direct evidence involving EV-associated lncRNAs and circRNAs in paediatric airway remodelling remains limited. The review therefore focuses on currently available mechanistic evidence, translational relevance, and major knowledge gaps.
EV-associated non-coding RNAs in paediatric asthma airway remodelling: current mechanistic evidence and therapeutic perspectives
Hu Gao

