{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T20:18:16Z","timestamp":1790713096340,"version":"4.1.0"},"reference-count":41,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2017,6,13]],"date-time":"2017-06-13T00:00:00Z","timestamp":1497312000000},"content-version":"vor","delay-in-days":0,"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":["81370421"],"award-info":[{"award-number":["81370421"]}],"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":["81370330"],"award-info":[{"award-number":["81370330"]}],"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":["81670344"],"award-info":[{"award-number":["81670344"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2017,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Endothelial cell dysfunction is one of the main reasons for type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> diabetes vascular complications. Hydrogen sulphide (H<jats:sub>2<\/jats:sub>S) has antioxidative effect, but its regulation on mitochondrial dynamics and mitophagy in aortic endothelial cells under hyperglycaemia and hyperlipidaemia is unclear. Rat aortic endothelial cells (<jats:styled-content style=\"fixed-case\">RAEC<\/jats:styled-content>s) were treated with 40 mM glucose and 200 \u03bcM palmitate to imitate endothelium under hyperglycaemia and hyperlipidaemia, and 100 \u03bcM Na<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> was used as an exogenous H<jats:sub>2<\/jats:sub>S donor. Firstly, we demonstrated that high glucose and palmitate decreased H<jats:sub>2<\/jats:sub>S production and <jats:styled-content style=\"fixed-case\">CSE<\/jats:styled-content> expression in <jats:styled-content style=\"fixed-case\">RAEC<\/jats:styled-content>s. Then, the antioxidative effect of H<jats:sub>2<\/jats:sub>S was proved in <jats:styled-content style=\"fixed-case\">RAEC<\/jats:styled-content>s under high glucose and palmitate to reduce mitochondrial <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> level. We also showed that exogenous H<jats:sub>2<\/jats:sub>S inhibited mitochondrial apoptosis in <jats:styled-content style=\"fixed-case\">RAEC<\/jats:styled-content>s under high glucose and palmitate. Using Mito Tracker and transmission electron microscopy assay, we revealed that exogenous H<jats:sub>2<\/jats:sub>S decreased mitochondrial fragments and significantly reduced the expression of p\u2010Drp\u20101\/Drp\u20101 and Fis1 compared to high\u2010glucose and high\u2010palmitate group, whereas it increased mitophagy by transmission electron microscopy assay. We demonstrated that exogenous H<jats:sub>2<\/jats:sub>S facilitated Parkin recruited by PINK1 by immunoprecipitation and immunostaining assays and then ubiquitylated mitofusin 2 (Mfn2), which illuminated the mechanism of exogenous H<jats:sub>2<\/jats:sub>S on mitophagy. Parkin si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> suppressed the expression of Mfn2, Nix and <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3B, which revealed that it eliminated mitophagy. In summary, exogenous H<jats:sub>2<\/jats:sub>S could protect <jats:styled-content style=\"fixed-case\">RAEC<\/jats:styled-content>s against apoptosis under high glucose and palmitate by suppressing oxidative stress, decreasing mitochondrial fragments and promoting mitophagy. Based on these results, we proposed a new mechanism of H<jats:sub>2<\/jats:sub>S on protecting endothelium, which might provide a new strategy for type <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> diabetes vascular complication.<\/jats:p>","DOI":"10.1111\/jcmm.13223","type":"journal-article","created":{"date-parts":[[2017,6,13]],"date-time":"2017-06-13T13:06:48Z","timestamp":1497359208000},"page":"3190-3203","source":"Crossref","is-referenced-by-count":66,"title":["Hydrogen Sulphide modulating mitochondrial morphology to promote mitophagy in endothelial cells under high\u2010glucose and high\u2010palmitate"],"prefix":"10.1111","volume":"21","author":[{"given":"Ning","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Pathophysiology Harbin Medical University Harbin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jichao","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology Harbin 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