Impact of Epigenetic Modifications in Airway Diseases. Role of Inflammation, Environmental Factors and Aging

Airway diseases, including asthma and chronic obstructive pulmonary disease (COPD) are global public health burden due to their high prevalence, morbidity, and mortality. Although these conditions are clinically distinct, they share key pathogenic mechanisms, including chronic inflammation, oxidative stress, and airway remodeling. Continuous exposure of the lungs to environmental agents and pathogens increases their susceptibility to injury and dysregulated immune responses, thereby promoting chronic disease progression. Environmental factors, including cigarette smoke and air pollution, can induce epigenetic changes that act as intermediaries between external insults and disease phenotypes. These epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs, regulate gene expression without altering the DNA sequence. By modulating chromatin structure and transcriptional activity, they influence immune function, lung homeostasis, and disease susceptibility, thereby contributing to persistent inflammation, airway remodeling, and variability in therapeutic responses.

Advances in epigenetics have led to the identification of novel biomarkers and potential therapeutic targets, offering new perspectives for diagnosis and treatment. We provide a comprehensive overview of the most recent advances in this field.

Current evidence and emerging insightsh discussed in this review might facilitate the understanding of how epigenetic alterations contribute to the biological mechanisms of respiratory diseases and help future research priorities.