ArticleCell cycle (Georgetown, Tex.)2020
Diminution of microRNA-98 alleviates renal fibrosis in diabetic nephropathy by elevating Nedd4L and inactivating TGF-β/Smad2/3 pathway.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 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
11 citing papers in PubMed, 15 citations in OpenAlex.
- Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024Review
- Expression of TNFR1, VEGFA, CD147 and MCT1 as early biomarkers of diabetes complications and the impact of aging on this profile.Scientific reports · 2023Article
- The miR-143/145 cluster induced by TGF-β1 suppresses Wilms' tumor 1 expression in cultured human podocytes.American journal of physiology. Renal physiology · 2023Article
- NEDD4L facilitates granulosa cell ferroptosis by promoting GPX4 ubiquitination and degradation.Endocrine connections · 2023Article
- Review
- Article
- MicroRNA-98-5p inhibits human mesangial cell proliferation and TNF-α and IL-6 secretion by targeting BTB and CNC homology 1.Experimental and therapeutic medicine · 2021Article
- Distinct associations of NEDD4L expression with genetic abnormalities and prognosis in acute myeloid leukemia.Cancer cell international · 2021Article
- MiR-142-3p ameliorates high glucose-induced renal tubular epithelial cell injury by targeting BOD1.Clinical and experimental nephrology · 2021Article
- Lower expression of Hsa_circRNA_102682 in diabetic hyperhomocysteinemia negatively related to creatinemia is associated with TGF-β and CTGF.Journal of clinical laboratory analysis · 2021Article
- Update on the Mechanisms of Tubular Cell Injury in Diabetic Kidney Disease.Frontiers in medicine · 2021Review
Corrections and comments
- Retraction · 2022-11-08Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Error in Data ·
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have already been documented to function in diabetic nephropathy (DN), yet little research has focused on the role of miR-98 in this disease. Here, we discuss the mechanism of miR-98 on the renal fibrosis in DN. Recombinant adeno-associated virus carrying miR-98 inhibitor or Nedd4L overexpression plasmid was injected into DN modeled rats to explore their roles in DN. Renal tubular epithelial cell injury models (NRK-52E cells) were induced by high glucose (HG). HG-treated NRK-52E cells were transfected with miR-98 inhibitor or Nedd4L overexpression plasmid for further verification. MiR-98 was upregulated, Nedd4L was downregulated and TGF-β/Smad2/3 signaling was activated in kidney tissues of DN rats and HG-treated NRK-52E cells. miR-98 targeted Nedd4L mRNA 3'UTR. MiR-98 depletion and Nedd4L overexpression inactivated TGF-β/Smad2/3 signaling pathway, alleviated pathological damage and fibrosis, ameliorated inflammation, and depressed cell apoptosis of kidney tissues of DN rats. MiR-98 depletion and Nedd4L overexpression inactivated TGF-β/Smad2/3 signaling pathway, strengthened viability, and limited apoptosis of HG-treated renal tubular epithelial cells. Nedd4L overexpression reversed the effect of up-regulating miR-98 on DN rats and HG-treated renal tubular epithelial cells. Altogether, we find that miR-98 is upregulated in kidney tissues of DN rats, and miR-98 diminution and Nedd4L elevation attenuate renal fibrosis through inactivation of the TGF-β/Smad2/3 pathway, which provides a novel therapy for DN.
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.