Sirtuins are a class of proteins that possess either mono-ADP-ribosyltransferase, or deacylase activity. Sirtuins have been implicated in influencing a wide range of cellular processes like aging, transcription, apoptosis, inflammation and stress resistance, as well as energy efficiency and alertness during low-calorie situations. Sirtuins can also control circadian clocks and mitochondrial biogenesis. Mammals possess seven sirtuins (SIRT1-7). SIRT6, a member of the Sir2 protein family, is known to have NAD+ dependent histone deacetylase, mono-ADP-ribotransferase and deadipoacylase catalysis. Through these functions, SIRT6 plays an important role in regulating DNA repair, telomere maintenance, inflammatory response and the occurrence and development of cancer. This paper reviews the role of SIRT6 in chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, asthma, non-small cell lung cancer, and other respiratory diseases. In terms of the pathogenesis of COPD, SIRT6 plays a role in lung aging, which is manifested in DNA damage, telomere shortening, and, autophagy. SIRT6 is involved in pulmonary epithelial-mesenchymal transition (EMT) in idiopathic pulmonary fibrosis, and it is resistant to intrapulmonary EMT induced by bleomycin, showing that the role of resistance to fibrosis. SIRT6 deacetylation can mediate the reduction of airway inflammation in bronchial asthma and also participate in the process of autoimmune inflammation. SIRT6 plays a key role in the formation and growth maintenance of NSCLC. Understanding the role of SIRT6 in the respiratory system is conducive to revealing the disease mechanism and exploring new therapeutic targets or developing new drugs.
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