ArticleInternational journal of biological sciences2021
NCTD Prevents Renal Interstitial Fibrosis via Targeting Sp1/lncRNA Gm26669 Axis.
Article in International journal of biological sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Berberine attenuates diabetic kidney injury via FOXO1/SP1-associated regulation of renal SGLT-2 expression.Chinese medicine · 2026Article
- Role of LncRNA in Pathogenesis, Diagnosis and Treatment of Chronic Kidney Disease.Cell biochemistry and biophysics · 2025Review
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Transcription Factors in the Pathogenesis of Lupus Nephritis and Their Targeted Therapy.International journal of molecular sciences · 2024Review
- Strategies for Solubility and Bioavailability Enhancement and Toxicity Reduction of Norcantharidin.Molecules (Basel, Switzerland) · 2022Review
- Comprehensive analyses of the microRNA-messenger RNA-transcription factor regulatory network in mouse and human renal fibrosis.Frontiers in genetics · 2022Article
- The Long Noncoding Transcript HNSCAT1 Activates KRT80 and Triggers Therapeutic Efficacy in Head and Neck Squamous Cell Carcinoma.Oxidative medicine and cellular longevity · 2022Article
- MicroRNA miR-4709-3p targets Large Tumor Suppressor Kinase 2 (LATS2) and induces obstructive renal fibrosis through Hippo signaling.Bioengineered · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous study, we demonstrated that norcantharidin (NCTD) is a potential therapeutic agent for renal interstitial fibrosis (RIF). Recently, we found that lncRNA Gm26669 (Gm26669) contributed to the development of RIF and could be regulated by NCTD. However, the upstream mechanisms of Gm26669 and whether the anti-RIF effects of NCTD are related to its regulatory action on Gm26669 remain unclear. Our bioinformatics analysis indicated that special protein1 (Sp1), a transcription factor, may bind to the promoter of Gm26669. In the present study, we observed a significant increase in the nuclear translocation of Sp1 using both
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