{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T12:35:36Z","timestamp":1788784536296,"version":"build-2803163510"},"reference-count":32,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,6,25]],"date-time":"2019-06-25T00:00:00Z","timestamp":1561420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,6,25]],"date-time":"2019-06-25T00:00:00Z","timestamp":1561420800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"name":"Clinical Key Specialty Construction Project in Fujian Province","award":["Min Wei Medical Letter [2015] No. 593"],"award-info":[{"award-number":["Min Wei Medical Letter [2015] No. 593"]}]},{"name":"Foundation of Nanjing Military Command of People's Liberation Army","award":["15MS135"],"award-info":[{"award-number":["15MS135"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Chronic obstructive pulmonary disease (COPD) is a major global epidemic with increasing incidence worldwide. The pathogenesis of COPD is involved with mitochondrial autophagy. Recently, it has been reported that FUN14 domain containing 1 (FUNDC1) is a mediator of mitochondrial autophagy. Therefore, we hypothesized that FUNDC1 was involved in cigarette smoke (CS)\u2010induced COPD progression by regulating mitochondrial autophagy. In vitro cigarette smoke extract (CSE)\u2010treated human bronchial epithelial cell (hBEC) Beas\u20102B cell line and in vivo CS\u2010induced COPD mouse models were developed, in which FUNDC1 expression was measured. Next, whether FUNDC1 interacted with dynamin\u2010related protein 1 (DRP1) in COPD was investigated. The functional mechanism of FUNDC1 in COPD was evaluated through gain\u2010 or loss\u2010of\u2010function studies. Then, pulmonary function, mitochondrial transmembrane potential (MTP) and mucociliary clearance (MCC) were examined. Levels of interleukin\u20106 (IL\u20106) and tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) and expression of autophagy\u2010specific markers (light chain 3 [LC3] II, LC3 I, and Tom20) were measured. Finally, apoptosis and mitochondrial autophagy were assessed. FUNDC1 was highly expressed in CSE\u2010treated hBECs and COPD mice. Meanwhile, FUNDC1 was proved to interact with DRP1 in CSE\u2010treated cells. Moreover, in CSE\u2010treated hBECs, silencing FUNDC1 was observed to reduce levels of IL\u20106 and TNF\u2010\u03b1, and MTP but increase MCC, and inhibit CSE\u2010induced mitochondrial autophagy and Beas\u20102B cell apoptosis, which was consistent with the trend in COPD mouse models. In addition, pulmonary function of COPD mouse models was increased in response to FUNDC1 silencing. Finally, silencing of DRP1 also inhibited mitochondrial autophagy and Beas\u20102B cell apoptosis. Collectively, FUNDC1 silencing could suppress the progression of COPD by inhibiting mitochondrial autophagy and hBEC apoptosis through interaction with DRP1, highlighting a potential therapeutic target for COPD treatment.<\/jats:p>","DOI":"10.1002\/jcb.29028","type":"journal-article","created":{"date-parts":[[2019,6,25]],"date-time":"2019-06-25T16:16:17Z","timestamp":1561479377000},"page":"17602-17615","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Silencing FUNDC1 alleviates chronic obstructive pulmonary disease by inhibiting mitochondrial autophagy and bronchial epithelium cell apoptosis under hypoxic environment"],"prefix":"10.1002","volume":"120","author":[{"given":"Wen","family":"Wen","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine Fuzhou General Hospital of Fujian Medical University, Dongfang Hospital of Xiamen University, 900th Hospital of the Joint Logistics Support Force  Fuzhou P.R. 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