ABSTRACT Bronchial asthma is a significant inflammatory disorder impacting the airways. While current therapeutic interventions manage these symptoms, they do not offer a cure for the condition. Emerging research indicates that specific microRNAs (miRNAs) are implicated in the pathogenesis of asthma and the associated airway remodeling. Notably, miR‐16‐5p has been identified as a regulator of TGF‐β1‐induced epithelial‐mesenchymal transition (EMT) in bronchial epithelial cells. This study investigates the influence of miR‐16‐5p on pulmonary function, inflammation, and fibrosis in asthma, focusing on its interaction with the TGF‐β1/Smad3 signaling pathway, using a rat model for experimental analysis. Male Sprague–Dawley rats were given ovalbumin (OVA) and aluminum hydroxide to create an asthma model. They were divided into six groups. miRNA treatments were delivered using PEG‐liposomes before each asthma challenge for 8 weeks. Asthma rats had lower levels of miR‐16‐5p. Elevating miR‐16‐5p levels improved breathing, reduced inflammation, and prevented lung damage. miR‐16‐5p regulated the TGF‐β1/Smad3 pathway by targeting Smad3, indicating its protective role against asthma. Increasing miR‐16‐5p levels can improve lung function, reduce inflammation, and prevent lung fibrosis in asthma rats by targeting Smad3 to block the TGF‐β1/Smad3 pathway. This finding suggests that miR‐16‐5p has translational potential as a novel therapeutic target for asthma treatment, which could lead to more effective strategies for asthma management in the future.
She et al. (Sun,) studied this question.
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