DNA repair and genomic stability in lungs affected by acute injury

Abstract Acute pulmonary injury, or acute respiratory distress syndrome, has a high incidence in elderly individuals and high mortality in its most severe degree, becoming a challenge to public health due to pathophysiological complications and increased economic burden. Acute pulmonary injury can develop from sepsis, septic shock, and pancreatitis causing reduction of alveolar airspace due to hyperinflammatory response. Oxidative stress acts directly on the maintenance of inflammation, resulting in tissue injury, as well as inducing DNA damages. Once the DNA is damaged, enzymatic DNA repair mechanisms act on lesions in order to maintain genomic stability and, consequently, contribute to cell viability and homeostasis. Although palliative treatment based on mechanical ventilation and antibiotic using have a kind of efficacy, therapies based on modulation of DNA repair and genomic stability could be effective for improving repair and recovery of lung tissue in patients with acute pulmonary injury.