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However, the molecular mechanism remains unclear. The mechanisms that underlie diabetic hyposalivation were studied by db\/db mice and SMG\u2010C6 cells. We found morphological changes and decreased stimulated salivary flow rates of the submandibular gland (SMG) in diabetic mice. We observed structural changes and dysfunction of mitochondria. More mitophagosomes and higher expression of autophagy\u2010related proteins were detected. Increased levels of proteins PINK1 and Parkin indicate that PINK1\/Parkin\u2010mediated mitophagy was activated in diabetic SMG. Consistently, high glucose (HG) induced mitochondrial dysfunction and PINK1\/Parkin\u2010mediated mitophagy in cultivated SMG\u2010C6 cells. HG also increased reactive oxygen species (ROS) and lessened activation of antioxidants in SMG\u2010C6 cells. In addition, HG lowered ERK1\/2 phosphorylation and HG\u2010induced mitophagy was decreased after ERK1\/2 was activated by LM22B\u201010. Altogether, these data suggest that ROS played a crucial role in diabetes\u2010induced mitochondrial dysfunction and PINK1\/Parkin\u2010mediated mitophagy and ERK1\/2 was required in HG\u2010induced mitophagy in SMG.<\/jats:p>","DOI":"10.1002\/jcp.28962","type":"journal-article","created":{"date-parts":[[2019,6,13]],"date-time":"2019-06-13T05:49:10Z","timestamp":1560404950000},"page":"232-244","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Type 2 diabetes\u2010induced hyposalivation of the submandibular gland through PINK1\/Parkin\u2010mediated mitophagy"],"prefix":"10.1002","volume":"235","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5935-1911","authenticated-orcid":false,"given":"Ruo\u2010Lan","family":"Xiang","sequence":"first","affiliation":[{"name":"Center for Salivary Gland Diseases of Peking University School and Hospital of Stomatology, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of 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