SIRT1 as a Potential Therapeutic Target for Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease characterized by irreversible airflow obstruction and lung function decline. It is well established that COPD represents a major cause of morbidity and mortality globally. Due to the substantial economic and social burdens associated with COPD, it is necessary to discover new targets and develop novel beneficial therapies. Although the pathogenesis of COPD is complex and remains to be robustly elucidated, numerous studies have shown that oxidative stress, inflammatory responses, cell apoptosis, autophagy, and aging are involved in the pathogenesis of COPD. Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase belonging to the silent information regulator 2 (Sir2) family. Multiple studies have indicated that SIRT1 plays an important role in oxidative stress, apoptosis, inflammation, autophagy, and cellular senescence, which contributes to the pathogenesis and development of COPD. This review aimed to discuss the functions and mechanisms of SIRT1 in the progression of COPD and concluded that SIRT1 activation might be a potential therapeutic strategy for COPD.

Automated summary

Chronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease characterized by irreversible airflow obstruction and lung function decline. SIRT1, a member of the Sir2 family, plays important roles in oxidative stress, apoptosis, inflammation, autophagy, and cellular senescence, which are involved in the pathogenesis and development of COPD. SIRT1 activation may be a potential therapeutic strategy for COPD.