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However, the mechanisms by which lipid accumulation leads to the development or progression of this disease have not been fully elucidated. In this work, we have identified a role for the rate\u2010limiting enzyme in lipolysis, adipose triglyceride lipase (<jats:styled-content style=\"fixed-case\">ATGL<\/jats:styled-content>; also called patatin\u2010like phospholipase domain\u2010containing protein 2), in renal lipid metabolism and kidney disease. <jats:styled-content style=\"fixed-case\">ATGL<\/jats:styled-content>\u2010deficient (<jats:italic>Atgl<\/jats:italic>(\u2212\/\u2212)) mice displayed albuminuria, accompanied by ectopic deposition of fat in the kidney. Magnetic resonance imaging demonstrated that the contrast agent gadopentetic acid was retained in kidney tissue, suggesting defects in the glomerular filtration barrier. Furthermore, transmission electron microscopy revealed lipid deposits in the podocyte, along with foot process fusion and morphological changes suggestive of apoptosis. Indeed, shRNA\u2010mediated depletion of <jats:styled-content style=\"fixed-case\">ATGL<\/jats:styled-content> promoted podocyte apoptosis, accompanied by increased levels of intracellular reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) and F\u2010actin fibre redistribution. These effects could be partially reversed by treatment with the antioxidant <jats:italic>N<\/jats:italic>\u2010acetylcysteine. These data suggest that <jats:styled-content style=\"fixed-case\">ATGL<\/jats:styled-content> deficiency induces renal lipid accumulation, proteinuria and glomerular filtration barrier dysfunction and implicate increased intracellular <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> levels in inducing podocyte F\u2010actin rearrangement, foot process fusion and apoptosis that underlie these pathological features.<\/jats:p><\/jats:sec><jats:sec><jats:title>Enzymes<\/jats:title><jats:p>Adipose triglyceride lipase, <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>3.1.1.3.<\/jats:p><\/jats:sec>","DOI":"10.1111\/febs.14038","type":"journal-article","created":{"date-parts":[[2017,2,14]],"date-time":"2017-02-14T07:32:45Z","timestamp":1487057565000},"page":"1070-1081","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["<i>Atgl<\/i> deficiency induces podocyte apoptosis and leads to glomerular filtration barrier damage"],"prefix":"10.1111","volume":"284","author":[{"given":"Wen","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Endocrinology Southwest Hospital Third Military Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youzhao","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Southwest Hospital Third Military Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Gynaecology and Obstetrics Daping Hospital Third Military Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiongyu","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Southwest Hospital State Key Laboratory of Trauma Burns and Combined Injury Third Military Medical 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