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However, whether Sidt2 is involved in the metabolic regulation in skeletal muscle remains unknown. In this study, for the first time, using skeletal muscle\u2010selective\n                    <jats:italic>Sidt2<\/jats:italic>\n                    knockout mice, we found that Sidt2 was vital for the quality control of mitochondria in mouse skeletal muscle. These mice showed significantly reduced muscle tolerance and structurally abnormal mitochondria. Deletion of the\n                    <jats:italic>Sidt2<\/jats:italic>\n                    gene resulted in decreased expression of mitochondrial fusion protein 2 (Mfn2) and Dynamin\u2010related protein 1 (Drp1), as well as peroxisome proliferator\u2010activated receptor \u03b3 coactivator\u20101 (PGC1\u2010\u03b1). In addition, the clearance of damaged mitochondria in skeletal muscle was inhibited upon\n                    <jats:italic>Sidt2<\/jats:italic>\n                    deletion, which was caused by blockade of autophagy flow. Mechanistically, the fusion of autophagosomes and lysosomes was compromised in\n                    <jats:italic>Sidt2<\/jats:italic>\n                    knockout skeletal muscle cells. In summary, the deletion of the\n                    <jats:italic>Sidt2<\/jats:italic>\n                    gene not only interfered with the quality control of mitochondria, but also inhibited the clearance of mitochondria and caused the accumulation of a large number of damaged mitochondria, ultimately leading to the abnormal structure and function of skeletal muscle.\n                  <\/jats:p>","DOI":"10.1096\/fj.202000424r","type":"journal-article","created":{"date-parts":[[2021,3,14]],"date-time":"2021-03-14T09:50:23Z","timestamp":1615715423000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["The lysosomal membrane protein Sidt2 is a vital regulator of mitochondrial quality control in skeletal muscle"],"prefix":"10.1096","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9011-0507","authenticated-orcid":false,"given":"Lizhuo","family":"Wang","sequence":"first","affiliation":[{"name":"Institute 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Clinical Medicine Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feiteng","family":"Liang","sequence":"additional","affiliation":[{"name":"School of Clinical Medicine Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fengbiao","family":"Tan","sequence":"additional","affiliation":[{"name":"Anhui Province Key Laboratory of Biological Macro\u2010molecules Research (Wannan Medical College) Wannan Medical College  Wuhu PR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Du","sequence":"additional","affiliation":[{"name":"Institute of Endocrine and Metabolic Diseases The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College)  Wuhu PR China"},{"name":"Department of Endocrinology and Genetic Metabolism The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College)  Wuhu 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