LncRNA SAL-RNA1 Knockdown Suppressed Pink1-Mediated Mitophagy Protects Against CS-Induced Alveolar Cells Senescence Through Regulation of Sirt1

Abstract Background LncRNAs pays an important roles in the regulation of alveolar cells in cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD). However, the role of lncRNA SAL-RNA1 in promoting mitophagy and reduces senescence of alveolar cells in COPD is unknow. Methods This study is aims to elucidate the underlying mechanism of LncRNA SAL-RNA1 and phosphatase and tensin homolog (PTEN)-induced putative protein kinase 1 (PINK1) expression were upregulated in alveolar of emphysema mice and CS treated alveolar epithelial cells. LncRNA SAL-RNA1 knockdown suppressed mitophagy and induced senescence of alveolar cells while overexpressing lncRNA SAL-RNA1 promoted mitophagy and reduced the senescence of alveolar cells. In addition, lncRNA SAL-RNA1 interacted with Sirt1 and regulated the upgradation of Sirt1. Results We further found lncRNA SAL-RNA1 regulated Pink1 expression through Sirt1. Mechanistically, lncRNA SAL-RNA1 regulated PinK1-mediated mitophagy and senescence of alveolar cells through regulation Sirt1. Conclusion Finally, overexpression lncRNA SAL-RNA1 promote mitophagy and relieved emphysema.