{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T19:16:08Z","timestamp":1778613368340,"version":"3.51.4"},"reference-count":51,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,6,15]],"date-time":"2021-06-15T00:00:00Z","timestamp":1623715200000},"content-version":"vor","delay-in-days":165,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81830001"],"award-info":[{"award-number":["81830001"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31871157"],"award-info":[{"award-number":["31871157"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p>This study investigated whether the mitochondrial\u2010targeted peptide SS\u201031 can protect against cigarette smoke\u2010 (CS\u2010) induced airway inflammation and oxidative stress <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>. Mice were exposed to CS for 4 weeks to establish a CS\u2010induced airway inflammation model, and those in the experimental group were pretreated with SS\u201031 1\u2009h before CS exposure. Pathologic changes and oxidative stress in lung tissue, inflammatory cell counts, and proinflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) were examined. The mechanistic basis for the effects of SS\u201031 on CS extract\u2010 (CSE\u2010) induced airway inflammation and oxidative stress was investigated using BEAS\u20102B bronchial epithelial cells and by RNA sequencing and western blot analysis of lung tissues. SS\u201031 attenuated CS\u2010induced inflammatory injury of the airway and reduced total cell, neutrophil, and macrophage counts and tumor necrosis factor\u2010 (TNF\u2010) <jats:italic>\u03b1<\/jats:italic>, interleukin\u2010 (IL\u2010) 6, and matrix metalloproteinase (MMP) 9 levels in BALF. SS\u201031 also attenuated CS\u2010induced oxidative stress by decreasing malondialdehyde (MDA) and myeloperoxidase (MPO) activities and increasing that of superoxide dismutase (SOD). It also reversed CS\u2010induced changes in the expression of mitochondrial fission protein (MFF) and optic atrophy (OPA) 1 and reduced the amount of cytochrome c released into the cytosol. Pretreatment with SS\u201031 normalized TNF\u2010<jats:italic>\u03b1<\/jats:italic>, IL\u20106, and MMP9 expression, MDA and SOD activities, and ROS generation in CSE\u2010treated BEAS\u20102B cells and reversed the changes in MFF and OPA1 expression. RNA sequencing and western blot analysis showed that SS\u201031 inhibited CS\u2010induced activation of the mitogen\u2010activated protein kinase (MAPK) signaling pathway <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic>. Thus, SS\u201031 alleviates CS\u2010induced airway inflammation and oxidative stress via modulation of mitochondrial function and regulation of MAPK signaling and thus has therapeutic potential for the treatment of airway disorders caused by smoking.<\/jats:p>","DOI":"10.1155\/2021\/6644238","type":"journal-article","created":{"date-parts":[[2021,6,15]],"date-time":"2021-06-15T23:20:55Z","timestamp":1623799255000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Mitochondrial\u2010Targeting Antioxidant SS\u201031 Suppresses Airway Inflammation and Oxidative Stress Induced by Cigarette 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