{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T02:14:59Z","timestamp":1789179299121,"version":"build-2803163510"},"reference-count":71,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:p>\n                    Maladaptive repair after AKI may lead to progressive fibrosis and decline in kidney function. Sphingosine 1-phosphate has an important role in kidney injury and pleiotropic effects in fibrosis. We investigated the involvement of sphingosine kinase 1 and 2 (SphK1 and SphK2), which phosphorylate sphingosine to produce sphingosine 1-phosphate, in kidney fibrosis induced by folic acid (FA) or unilateral ischemia-reperfusion injury. Analysis of Masson trichrome staining and fibrotic marker protein and mRNA expression 14 days after AKI revealed that wild-type (WT) and\n                    <jats:italic toggle=\"yes\">Sphk1\u2212\/\u2212<\/jats:italic>\n                    mice exhibited more kidney fibrosis than\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    mice. Furthermore, kidneys of FA-treated WT and\n                    <jats:italic toggle=\"yes\">Sphk1\u2212\/\u2212<\/jats:italic>\n                    mice had greater immune cell infiltration and expression of fibrotic and inflammatory markers than kidneys of FA-treated\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    mice. In contrast, kidneys of\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    mice exhibited greater expression of\n                    <jats:italic toggle=\"yes\">Ifng<\/jats:italic>\n                    and IFN-\n                    <jats:italic toggle=\"yes\">\u03b3<\/jats:italic>\n                    \u2013responsive genes (\n                    <jats:italic toggle=\"yes\">Cxcl9<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">Cxcl10<\/jats:italic>\n                    ) than kidneys of WT or\n                    <jats:italic toggle=\"yes\">Sphk1\u2212\/\u2212<\/jats:italic>\n                    mice did at this time point. Splenic T cells from untreated\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    mice were hyperproliferative and produced more IFN-\n                    <jats:italic toggle=\"yes\">\u03b3<\/jats:italic>\n                    than did those of WT or\n                    <jats:italic toggle=\"yes\">Sphk1\u2212\/\u2212<\/jats:italic>\n                    mice. IFN-\n                    <jats:italic toggle=\"yes\">\u03b3<\/jats:italic>\n                    blocking antibody administered to\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    mice or deletion of\n                    <jats:italic toggle=\"yes\">Ifng<\/jats:italic>\n                    (\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212Ifng\u2212\/\u2212<\/jats:italic>\n                    mice) blocked the protective effect of SphK2 deficiency in fibrosis. Moreover, adoptive transfer of\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212<\/jats:italic>\n                    (but not\n                    <jats:italic toggle=\"yes\">Sphk2\u2212\/\u2212Ifng\u2212\/\u2212<\/jats:italic>\n                    ) CD4 T cells into WT mice blocked FA-induced fibrosis. Finally, a selective SphK2 inhibitor blocked FA-induced kidney fibrosis in WT mice. These studies demonstrate that SphK2 inhibition may serve as a novel therapeutic approach for attenuating kidney fibrosis.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016030306","type":"journal-article","created":{"date-parts":[[2016,10,31]],"date-time":"2016-10-31T21:41:06Z","timestamp":1477950066000},"page":"1145-1161","source":"Crossref","is-referenced-by-count":68,"title":["Sphingosine Kinase 2 Deficiency Attenuates Kidney Fibrosis via IFN-\u03b3"],"prefix":"10.1681","volume":"28","author":[{"given":"Amandeep","family":"Bajwa","sequence":"first","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liping","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elvira","family":"Kurmaeva","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Ye","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krishna R.","family":"Dondeti","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Piotr","family":"Chroscicki","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leah S.","family":"Foley","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Z. Ayoade","family":"Balogun","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyle J.","family":"Alexander","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hojung","family":"Park","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin R.","family":"Lynch","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia, Charlottesville, Virginia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane L.","family":"Rosin","sequence":"additional","affiliation":[{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"},{"name":"Department of Pharmacology, University of Virginia, Charlottesville, Virginia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark D.","family":"Okusa","sequence":"additional","affiliation":[{"name":"Division of Nephrology,"},{"name":"Center for Immunity, Inflammation and Regenerative Medicine, Department of Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2016,10,31]]},"reference":[{"key":"B1-20230829","doi-asserted-by":"crossref","first-page":"F1078","DOI":"10.1152\/ajprenal.00017.2010","article-title":"Acute kidney injury: A springboard for progression in chronic kidney disease.","volume":"298","author":"Venkatachalam","year":"2010","journal-title":"Am 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