{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T03:50:11Z","timestamp":1789617011424,"version":"build-2803163510"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,12]]},"abstract":"<jats:p>\n                    Diabetic nephropathy is characterized by persistent albuminuria, progressive decline in GFR, and secondary hypertension. MicroRNAs are dysregulated in diabetic nephropathy, but identification of the specific microRNAs involved remains incomplete. Here, we show that the peripheral blood from patients with diabetes and the kidneys of animals with type 1 or 2 diabetes have low levels of microRNA-25 (miR-25) compared with those of their nondiabetic counterparts. Furthermore, treatment with high glucose decreased the expression of miR-25 in cultured kidney cells. In\n                    <jats:italic toggle=\"yes\">db<\/jats:italic>\n                    \/\n                    <jats:italic toggle=\"yes\">db<\/jats:italic>\n                    mice, systemic administration of an miR-25 agomir repressed glomerular fibrosis and reduced high BP. Notably, knockdown of miR-25 in normal mice by systemic administration of an miR-25 antagomir resulted in increased proteinuria, extracellular matrix accumulation, podocyte foot process effacement, and hypertension with renin-angiotensin system activation. However, excessive miR-25 did not cause kidney dysfunction in wild-type mice. RNA sequencing showed the alteration of miR-25 target genes in antagomir-treated mice, including the Ras-related gene CDC42.\n                    <jats:italic toggle=\"yes\">In vitro<\/jats:italic>\n                    , cotransfection with the miR-25 antagomir repressed luciferase activity from a reporter construct containing the CDC42 3\u2032 untranslated region. In conclusion, these results reveal a role for miR-25 in diabetic nephropathy and indicate a potential novel therapeutic target for this disease.\n                  <\/jats:p>","DOI":"10.1681\/asn.2015091017","type":"journal-article","created":{"date-parts":[[2017,9,18]],"date-time":"2017-09-18T20:55:22Z","timestamp":1505768122000},"page":"3627-3638","source":"Crossref","is-referenced-by-count":52,"title":["Variations in MicroRNA-25 Expression Influence the Severity of Diabetic Kidney Disease"],"prefix":"10.1681","volume":"28","author":[{"given":"Yunshuang","family":"Liu","sequence":"first","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"},{"name":"Clinical Laboratory of Hong Qi Hospital, Mudanjiang Medical University, Heilongjiang, People\u2019s Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongzhi","family":"Li","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jieting","family":"Liu","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pengfei","family":"Han","sequence":"additional","affiliation":[{"name":"Clinical Laboratory of Hong Qi Hospital, Mudanjiang Medical University, Heilongjiang, People\u2019s Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuefeng","family":"Li","sequence":"additional","affiliation":[{"name":"Clinical Laboratory of Hong Qi Hospital, Mudanjiang Medical University, Heilongjiang, People\u2019s Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"He","family":"Bai","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunlei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuelian","family":"Sun","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanjie","family":"Teng","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yufei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy, Medical Research Center, Heilongjiang, People\u2019s Republic of China; 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