ArticleJournal of diabetes investigation2023
LncRNA TCF7 contributes to high glucose-induced damage in human podocytes by up-regulating SEMA3A via sponging miR-16-5p.
Article in Journal of diabetes investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Silencing LncRNA SNHG14 alleviates renal tubular injury via the miR-483-5p/HDAC4 axis in diabetic kidney disease.Hormones (Athens, Greece) · 2025Article
- Research progress on non-coding RNA regulatory networks and targeted therapy in diabetic nephropathy.Frontiers in endocrinology · 2025Review
- The potential role of differentially expressed tRNA-derived fragments in high glucose-induced podocytes.Renal failure · 2024Article
- Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.Cell communication and signaling : CCS · 2024Review
- Role of Semaphorin 3A in Kidney Development and Diseases.Diagnostics (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AIMS/
introductionLong non-coding RNAs (lncRNAs) exert essential functions in the pathogenesis of diabetic nephropathy (DN). LncRNA T-cell factor 7 (TCF7) and semaphorin-3A (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. MATERIALS AND
methodsTCF7, miR-16-5p, and SEMA3A were quantified by a qRT-PCR or immunoblotting method. A CCK-8 assay gauged the cell viability. Measurement of cell apoptosis was done using flow cytometry. RNA immunoprecipitation (RIP), dual-luciferase reporter, and RNA pull-down assays were utilized to assay the targeted interactions among the variables.
resultsThe TCF7 and SEMA3A levels were elevated in serum from patients with diabetic nephropathy. TCF7 silencing or SEMA3A depletion ameliorated high glucose (HG)-induced podocyte injury. Moreover, TCF7 silencing protected against HG-induced podocyte injury by down-regulating SEMA3A. TCF7 targeted miR-16-5p, and miR-16-5p targeted SEMA3A. Furthermore, TCF7 affected the expression of SEMA3A by competing specifically for shared miR-16-5p.
conclusionsThese findings suggested that TCF7 silencing attenuated high glucose-induced podocyte damage partially through the miR-16-5p/SEMA3A regulation cascade.
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