ArticleAmerican journal of translational research2019
Sphingosine kinase 1 inhibition decreases the epithelial-mesenchymal transition and ameliorates renal fibrosis via modulating NF-κB signaling.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 13 citations in OpenAlex.
- The role of mesenchymal stem cells in IgA nephropathy: current evidence and future directions.Stem cell research & therapy · 2026Review
- Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025Review
- Epithelial-to-mesenchymal transition and live cell extrusion contribute to measles virus release from human airway epithelia.Journal of virology · 2025Article
- Article
- Identifying the mechanisms and molecular targets of Hongjingtian injection on treatment of TGFβ1-induced HK-2 cells: coupling network pharmacology with experimental verification.Annals of translational medicine · 2022Article
- SENP6 induces microglial polarization and neuroinflammation through de-SUMOylation of Annexin-A1 after cerebral ischaemia-reperfusion injury.Cell & bioscience · 2022Article
- Bone marrow mesenchymal stem cell-derived extracellular vesicles containing miR-181d protect rats against renal fibrosis by inhibiting KLF6 and the NF-κB signaling pathway.Cell death & disease · 2022Article
- A Rheostat of Ceramide and Sphingosine-1-Phosphate as a Determinant of Oxidative Stress-Mediated Kidney Injury.International journal of molecular sciences · 2022Review
- Asiaticoside inhibits epithelial-mesenchymal transition and stem cell-like properties of pancreatic cancer PANC-1 cells by blocking the activation of p65 and p38MAPK.Journal of gastrointestinal oncology · 2021Article
- Activation of the Cholinergic Anti-inflammatory Pathway Attenuated Angiotension II-Dependent Hypertension and Renal Injury.Frontiers in pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal fibrosis is a critical process underlying the development progression of chronic kidney disease to end-stage renal disease, which has intrigued much attention. This study aimed to investigate the role of Sphingosine kinase 1 (SphK1) on epithelial-mesenchymal transition (EMT) in renal fibrosis and the potential regulatory mechanisms. In the present study, unilateral ureteral obstruction (UUO)-induced mouse renal fibrosis model was established. HE and Masson staining were employed to detect the pathological change and fibrous deposition in renal tissues respectively. Moreover, the expression of SphK1, EMT relative proteins including E-cadherin (E-cad), N-cadherin (N-cad) and vimentin as well as fibrosis marker protein α-smooth muscle actin (α-SMA) were measured by immunohistochemistry and Western blot, respectively. In vitro, SphK1 silencing was generated in TGF-β induced human renal tubular epithelial HK-2 cells. Immunofluorescence staining was applied to examine the expression of α-SMA, then the levels of EMT relative proteins and NF-κB signaling were measured using Western blot. The results revealed that notably tubulointerstitial damage and fibrous deposition were detected in the UUO mouse renal tissues. The expression level of E-cad and SphK1 were decreased coupled with an increase of N-cad, vimentin and α-SMA expression. Furthermore, after knockdown of SphK1 in TGF-β induced HK-2 cells, the E-cad expression was up-regulated while N-cad, vimentin and α-SMA expression were down-regulated remarkably. In addition, the expression levels of phospho-NF-κB p65 (p-NF-κB p65) and p-IκB-α were lowered significantly following SphK1 silencing. These findings indicated that the inhibition of SphK1 protected renal tubular epithelial cells against renal fibrosis, by contribution to decrease the EMT via blocking the NF-κB signaling. Therefore, SphK1 may serve as a therapeutic target in the future.
Indexed as
Identifiers
31632556PMC6789211W2981785373What 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.