ArticleGene therapy2020
LncRNA SNHG16 induces proliferation and fibrogenesis via modulating miR-141-3p and CCND1 in diabetic nephropathy.
Article in Gene therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- Long Non-Coding RNAs and Micro RNAs in Chronic Kidney Disease: Recent Advances and Future Directions-A 5-Year Systematic Review.Life (Basel, Switzerland) · 2026Review
- Mechanistic insights into Shenqi Dihuang decoction in the treatment of immunoglobulin a nephropathy.Frontiers in pharmacology · 2025Article
- LncRNA SNHG14 silencing attenuates the progression of diabetic nephropathy via the miR-30e-5p/SOX4 axis.Journal of diabetes · 2024Article
- Silencing LncRNA SNHG16 suppresses the diabetic inflammatory response by targeting the miR-212-3p/NF-κB signaling pathway.Diabetology & metabolic syndrome · 2023Article
- LncRNA SNHG16 regulates RAS and NF-κB pathway-mediated NLRP3 inflammasome activation to aggravate diabetes nephropathy through stabilizing TLR4.Acta diabetologica · 2023Article
- Platyconic acid A‑induced PPM1A upregulation inhibits the proliferation, inflammation and extracellular matrix deposition of TGF‑β1‑induced lung fibroblasts.Molecular medicine reports · 2022Article
- Long non-coding RNAWorld journal of stem cells · 2022Article
- Long noncoding RNA PVT1 regulates the proliferation and apoptosis of ARPE-19 cellsCell cycle (Georgetown, Tex.) · 2022Article
- Regulation of Oxidative Stress by Long Non-Coding RNAs in Vascular Complications of Diabetes.Life (Basel, Switzerland) · 2022Review
- Long Non-Coding NONRATG001910.2 Promotes the Proliferation of Rat Mesangial Cell Line HBZY-1 Through the miR-339-3p/CTNNB1 Axis.Frontiers in genetics · 2022Article
- Article
- SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axis in vitro.Bioscience reports · 2021Article
- Prediction of a Competing Endogenous RNA Co-expression Network by Comprehensive Methods in Systemic Sclerosis-Related Interstitial Lung Disease.Frontiers in genetics · 2021Article
- Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LncRNAs are reported to participate in the progression of various diseases including diabetic nephropathy. Currently, we reported that SNHG16 was obviously upregulated in db/db mice and high glucose-treated mice mesangial cells. Then, functional experiments showed that SNHG16 silencing significantly inhibited proliferation of mice mesangial cells, which induced the apoptosis and triggered cell cycle arrest. Meanwhile, proliferation-related biomarkers PCNA and Cyclin D1 (CCND1) were greatly repressed. Furthermore, western blot analysis was conducted to test fibrogenesis-associated genes Fibronectin and α-SMA. Meanwhile, the increased protein expression levels of Fibronectin and α-SMA under high glucose conditions were reversed by loss of SNHG16. miR-141-3p has been reported to be involved in various diseases. Then, RNA immunoprecipitation assay revealed the relation between SNHG16 and miR-141-3p. Downregulation of SNHG16 was able to induce expression of miR-141-3p, which was obviously reduced in db/db diabetic nephropathy mice. In addition, CCND1 is a crucial cell cycle master in human diseases. CCND1 was speculated as the target of miR-141-3p and miR-141-3p inhibited CCND1 expression significantly. Meanwhile, we observed that loss of CCND1 greatly repressed mice mesangial cell proliferation and induced cell apoptosis. Taken these together, we revealed for the first time that SNHG16 induced proliferation and fibrogenesis via modulating miR-141-3p and CCND1 in diabetic nephropathy. SNHG16/miR-141-3p/CCND1 axis can suggest a pathological mechanism of progression of diabetic nephropathy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.