Targeting DNA damage: an important strategy for the prevention and treatment of respiratory diseases

DNA damage is one of the key factors that trigger respiratory system-related diseases. In recent years, the crucial role of DNA damage and repair mechanisms in the occurrence and development of lung diseases has been gradually revealed. DNA damage is not only closely related to the onset of lung diseases but also affects the disease process by regulating various biological processes such as cellular senescence, apoptosis, inflammatory responses, and vascular remodeling. This is particularly evident in common lung diseases such as asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and lung cancer, where the relationship between DNA damage and dysfunction of lung tissue cells has become increasingly prominent. This cellular response engages a coordinated network of DNA repair pathways, notably homologous recombination (HR) and non-homologous end joining (NHEJ) for resolving double-strand breaks, alongside base excision repair (BER) for small oxidative or alkylative lesions and nucleotide excision repair (NER) for bulky helix-distorting adducts, which play a vital role in maintaining genomic stability of lung cells and inhibiting disease progression. Therefore, this article describes the main types of DNA damage, repair pathways, and their mechanisms of action in lung diseases, and explores the research progress of therapeutic strategies targeting DNA damage repair mechanisms in respiratory system diseases. Through a deeper understanding of these mechanisms, new targeted and intervention directions for the treatment of respiratory system diseases may be provided in the future.