ArticleInternational journal of molecular medicine2018
Sphingomyelin synthase 2 promotes H2O2-induced endothelial dysfunction by activating the Wnt/β-catenin signaling pathway.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Sphingolipids and Atherosclerosis.Current atherosclerosis reports · 2026Review
- UCHL3 Promotes Triple-Negative Breast Cancer Metastatic Potential Through Enhancing Cell Migration and Invasion.Applied biochemistry and biotechnology · 2026Article
- Sphingolipid metabolites involved in the pathogenesis of atherosclerosis: perspectives on sphingolipids in atherosclerosis.Cellular & molecular biology letters · 2025Review
- Plasma Lipidomics Profiles Highlight the Associations of the Dual Antioxidant/Pro-oxidant Molecules Sphingomyelin and Phosphatidylcholine with Subclinical Atherosclerosis in Patients with Type 1 Diabetes.Antioxidants (Basel, Switzerland) · 2023Article
- The Effect of Cholesterol Efflux on Endothelial Dysfunction Caused by Oxidative Stress.International journal of molecular sciences · 2023Article
- A Rheostat of Ceramide and Sphingosine-1-Phosphate as a Determinant of Oxidative Stress-Mediated Kidney Injury.International journal of molecular sciences · 2022Review
- Sphingomyelin synthase 2 is a positive regulator of the CSF1R-STAT3 pathway in pancreatic cancer-associated macrophage.Frontiers in pharmacology · 2022Article
- Ceramide/Sphingomyelin Rheostat Regulated by Sphingomyelin Synthases and Chronic Diseases in Murine Models.Journal of lipid and atherosclerosis · 2020Review
- Fingolimod Affects Transcription of Genes Encoding Enzymes of Ceramide Metabolism in Animal Model of Alzheimer's Disease.Molecular neurobiology · 2020Article
- Simvastatin promotes endothelial dysfunction by activating the Wnt/β‑catenin pathway under oxidative stress.International journal of molecular medicine · 2019Article
- Sphingomyelin Synthase 2 Promotes Endothelial Dysfunction by Inducing Endoplasmic Reticulum Stress.International journal of molecular sciences · 2019Article
- Simvastatin Attenuates HMolecules (Basel, Switzerland) · 2019Article
- miR-33 and RIP140 participate in LPS-induced acute lung injuryTurkish journal of medical sciences · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is the primary cause of various cardiovascular and cerebrovascular diseases and has high morbidity and mortality rates. Oxidative stress‑induced endothelial cells (ECs) dysfunction is the pathological basis of AS. In addition, sphingomyelin (SM) and the Wnt/β‑catenin signaling pathway are considered to be closely associated with AS; however, the specific mechanism is not clear. Therefore, the present study investigated whether SM may induce ECs dysfunction through the Wnt/β‑catenin signaling pathway. Firstly, a sphingomyelin synthase 2 (SMS2) overexpression cell model was constructed. It was identified that the expression of SMS2 was increased when ECs were treated with H2O2. In addition, these results demonstrated that SMS2 overexpression promoted apoptosis and macrophage adhesion of H2O2‑induced ECs, thereby increasing the expression of β‑catenin. Furthermore, SMS activity was inhibited with Dy105, combined with simultaneous treatment with LiCl or H2O2. This additionally confirmed that Dy105 significantly inhibited SMS activity and decreased the level of ECs dysfunction and β‑catenin content; however, LiCl served a key role in activating the Wnt/β‑catenin signaling pathway to promote ECs dysfunction. Collectively, these results suggested that SMS2 overexpression may promote ECs dysfunction by activating the Wnt/β‑catenin signaling pathway, while Dy105 may inhibit the evolution of oxidative stress‑induced dysfunction.
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