{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T20:21:09Z","timestamp":1790626869673,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,12,29]],"date-time":"2022-12-29T00:00:00Z","timestamp":1672272000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims\/Introduction<\/jats:title><jats:p>Long non\u2010coding RNAs (lncRNAs) exert essential functions in the pathogenesis of diabetic nephropathy (DN). LncRNA T\u2010cell factor 7 (TCF7) and semaphorin\u20103A (SEMA3A) have been found to be involved in the progression of diabetic nephropathy. However, whether the effect of TCF7 on the pathogenesis of diabetic nephropathy is mediated by SEMA3A remains unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>TCF7, miR\u201016\u20105p, and SEMA3A were quantified by a qRT\u2010PCR or immunoblotting method. A CCK\u20108 assay gauged the cell viability. Measurement of cell apoptosis was done using flow cytometry. RNA immunoprecipitation (RIP), dual\u2010luciferase reporter, and RNA pull\u2010down assays were utilized to assay the targeted interactions among the variables.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The TCF7 and SEMA3A levels were elevated in serum from patients with diabetic nephropathy. TCF7 silencing or SEMA3A depletion ameliorated high glucose (HG)\u2010induced podocyte injury. Moreover, TCF7 silencing protected against HG\u2010induced podocyte injury by down\u2010regulating SEMA3A. TCF7 targeted miR\u201016\u20105p, and miR\u201016\u20105p targeted SEMA3A. Furthermore, TCF7 affected the expression of SEMA3A by competing specifically for shared miR\u201016\u20105p.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These findings suggested that TCF7 silencing attenuated high glucose\u2010induced podocyte damage partially through the miR\u201016\u20105p\/SEMA3A regulation cascade.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdi.13904","type":"journal-article","created":{"date-parts":[[2022,12,30]],"date-time":"2022-12-30T07:20:49Z","timestamp":1672384849000},"page":"193-204","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["<scp>LncRNA TCF7<\/scp> contributes to high glucose\u2010induced damage in human podocytes by up\u2010regulating <scp>SEMA3A<\/scp><i>via<\/i> sponging <scp>miR<\/scp>\u201016\u20105p"],"prefix":"10.1111","volume":"14","author":[{"given":"Zhenzhen","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of 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