Mechanisms and therapeutic strategies of asthma: from bench to bedside

Asthma is a heterogeneous chronic airway disease arising from a complex interplay of genetic susceptibility and environmental exposures. Key pathobiological features include dysregulated immune responses (particularly type 2 inflammation), structural airway remodeling, and mucus hypersecretion. Recent advances have illuminated mechanisms from epithelial "alarmin" cytokine release (TSLP, IL-33, IL-25) to downstream cellular networks involving Th2/Th17 lymphocytes, group 2 innate lymphoid cells (ILC2s), eosinophils, and mast cells. These pathways converge on bronchial hyperresponsiveness and airflow obstruction. Traditional therapy with inhaled corticosteroids and bronchodilators has improved asthma control, yet many patients, especially those with non-type 2-driven endotypes such as neutrophilic or obesity-related asthma, remain suboptimally controlled. This limitation has driven the development of precision medicine approaches that target specific cytokines and signaling cascades, including IgE, IL-5, IL-4/13, and TSLP, as well as intracellular signaling processes such as JAK-STAT. Parallel innovations in biomarkers such as FeNO, blood eosinophils, periostin, and multi-omics-based signatures facilitate patient stratification and prediction of treatment response. This comprehensive review synthesizes current knowledge from genetic and epigenetic foundations of asthma, through immunologic and neurogenic mechanisms, to translational advances in therapeutics from laboratory to clinic. We highlight the importance of endotyping and "treatable traits" such as eosinophilia, mucus plugging, or small-airway dysfunction in guiding individualized therapy. The emerging paradigm aims not only for symptom control but also for disease modification and remission, leveraging biomarkers and multidisciplinary approaches to achieve long-term asthma control in a broad patient population.