{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:30:03Z","timestamp":1786480203667,"version":"build-2736575974"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","funder":[{"DOI":"10.13039\/spuvm4mhooyg","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["16H05114"],"award-info":[{"award-number":["16H05114"]}],"id":[{"id":"10.13039\/spuvm4mhooyg","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/spuvm4mhooyg","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["20H03406"],"award-info":[{"award-number":["20H03406"]}],"id":[{"id":"10.13039\/spuvm4mhooyg","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/spuvm4mhooyg","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["17J11624"],"award-info":[{"award-number":["17J11624"]}],"id":[{"id":"10.13039\/spuvm4mhooyg","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Renal proximal tubulopathy plays a crucial role in kidney disease, but its molecular mechanism is incompletely understood. Because proximal tubular cells consume a lot of energy during reabsorption, the relationship between fatty acids (FAs) and proximal tubulopathy has been attracting attention. The purpose of this study is to investigate the association between change in renal FA composition and tubulopathy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice with cisplatin-induced nephrotoxicity were used as a model of AKI and 5\/6-nephrectomized mice were used as a model of CKD. Renal FA composition in mice was measured by GC-MS. Human tubular epithelial cells (HK-2 cells) were used for\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      studies.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In kidneys of AKI mice, increased stearic acid (C18:0) and decreased palmitic acid (C16:0) were observed, accompanied by increased expression of the long-chain FA elongase Elovl6. Similar results were also obtained in CKD mice. We show that C18:0 has higher tubular toxicity than C16:0\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      induction of ER stress. Using adenovirus-expressing Elovl6 or siRNA for Elovl6 in HK-2 cells, we demonstrated that increased Elovl6 expression contributes to tubulopathy\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      increasing C18:0. Elovl6 knockout suppressed the increased serum creatinine levels, renal ER stress, and inflammation that would usually result after 5\/6 nephrectomy. Advanced oxidation protein products (AOPPs), specifically an oxidized albumin, was found to induce Elovl6\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      the mTORC1\/SREBP1 pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      AOPPs may contribute to renal tubulopathy\n                      <jats:italic toggle=\"yes\">via<\/jats:italic>\n                      perturbation of renal FAs through induction of Elovl6. The perturbation of renal FAs induced by the AOPPs-Elovl6 system could be a potential target for the treatment of tubulopathy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0000772019","type":"journal-article","created":{"date-parts":[[2020,6,3]],"date-time":"2020-06-03T18:51:51Z","timestamp":1591210311000},"page":"781-796","source":"Crossref","is-referenced-by-count":11,"title":["Advanced Oxidation Protein Products Contribute to Renal Tubulopathy via Perturbation of Renal Fatty Acids"],"prefix":"10.34067","volume":"1","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1961-2472","authenticated-orcid":false,"given":"Tadashi","family":"Imafuku","sequence":"first","affiliation":[{"name":"Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan"},{"name":"Program for Leading Graduate Schools \u201cHIGO (Health Life Science: Interdisciplinary and Glocal Oriented) Program,\u201d Kumamoto University, Kumamoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Watanabe","sequence":"additional","affiliation":[{"name":"Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takao","family":"Satoh","sequence":"additional","affiliation":[{"name":"Kumamoto Industrial Research Institute, Kumamoto, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Matsuzaka","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki, Japan"},{"name":"Transborder Medical Research Center, University of Tsukuba, Ibaraki, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoaki","family":"Inazumi","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical 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