Cellular and Molecular Insights into the Pathophysiology of Obesity-Related Asthma

Obesity-related asthma is a distinct clinical phenotype, characterized by severe respiratory symptoms, reduced responsiveness to conventional glucocorticoid therapy, and a significantly increase in disease burden. With the rising global prevalence of obesity, the number of individuals affected by obesity-related asthma is steadily growing, presenting a pressing public health issue. The pathogenesis of obesity-related asthma is multifactorial, involving a complex interplay of metabolic and immune pathways. Key mechanisms include dysregulated T-cell differentiation, pro-inflammatory macrophage polarization, oxidative stress, and altered cytokines and adipokines secretion, all contributing to airway inflammation and remodeling. Additionally, metabolic factors, such as adiposity and adipokine imbalance, further complicated disease progression. A major clinical challenge is developing targeted therapies to address the substantial heterogeneity in this patient population. Current treatment approaches, largely focused on corticosteroids, often fail to achieve satisfactory outcomes, emphasizing the need for novel, tailored therapies that target the specific pathophysiological features of obesity-related asthma. This review systematically explores the cellular and molecular mechanisms driving obesity-related asthma, focusing on how obesity-associated factors such as adipokines and airway remodeling influence disease progression. The review also evaluates emerging therapeutic interventions and highlights the ongoing challenges in clinical diagnosis and management. By synthesizing recent research, this study aims to provide insights into potential strategies for improving treatment and clinical outcomes for patients with obesity-related asthma.