Document Type : Review article
Authors
1
Department of Cellular and Molecular Biology, Faculty of Advanced Sciences and Technology, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran.
2
Department of Health Equity, Immunoregulation Research Center, Shahed University, Tehran, Iran.
3
Department of Basic Sciences, Faculty of Veterinary Medicine, Shahrekord University, Shahrekord, Iran.
4
Immunoregulation Research Center, Shahed University, Tehran, Iran.
Abstract
The respiratory system is continually exposed to various harmful agents, which is why DNA repair is required. This comprises injury, inflammation, and other contents that are toxic and can cause damage to its genes. To eliminate the impact of DNA damage and restore cellular function, three pathways of repair are induced as follows: base excision repair, nucleotide excision repair (NER), and double-strand break pathway. However, such healing responses can be downregulated by long-term or severe injuries resulting in decreased recovery ability and predisposition to various diseases, such as lung cancer, chronic obstructive pulmonary disease (COPD), and fibrosis of the lungs. The generation of reactive oxygen species (ROS) during inflammation alters DNA and damages tissues. Despite this, inflammation will affect the initiation of tissue repair as well as DNA damage through the creation of ROS in this intricate process that occurs partly through innate immune responses and cytokine signaling. Cytotoxic processes hamper these fixing pathways of damaged genetic materials by inhibiting enzymes involved in DNA reparations and genes linked to repairs, thereby enhancing the risks of mutagenesis, carcinogenesis, and progressive diseases. Hence, the relationship between DNA repair and inflammatory reactions is crucial for lung health. It plays a major role in the pathophysiology of illnesses, such as cancer, COPD, fibrosis, and asthma. Inflammation and DNA damage are positively associated because they form a positive feedback loop that promotes disease and tissue pathology progression. DNA injury activates inflammation because immune cells are attracted to the site of injury, which in turn produces more oxidant molecules damaging the DNA. The evaluation of this relationship may help find approaches for reducing DNA damage, protecting genomic integrity, and preventing the progression of respiratory diseases.
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