ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Transforming Growth Factor β1 (TGF-β1) Appears to Promote Coronary Artery Disease by Upregulating Sphingosine Kinase 1 (SPHK1) and Further Upregulating Its Downstream TIMP-1.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- LncRNA uc003pxg.1 Interacts With miR-339-5p Promote Vascular Endothelial Cell Proliferation, Migration and Angiogenesis.Korean circulation journal · 2025Article
- A multi-omics approach identifies the key role of disorders of sphingolipid metabolism in Ang II-induced hypertensive cardiomyopathy myocardial remodeling.Scientific reports · 2024Article
- Gene therapy with AAV9-SGPL1 in an animal model of lung fibrosis.The Journal of pathology · 2024Article
- Integrative roles of sphingosine kinase in liver pathophysiology.Toxicological research · 2023Review
- Review
- Melatonin and TGF-β-Mediated Release of Extracellular Vesicles.Metabolites · 2023Review
- Development of Machine Learning Tools for Predicting Coronary Artery Disease in the Chinese Population.Disease markers · 2022Article
- Review
- Do exosomes play role in cardiovascular disease development in hematological malignancy?Molecular biology reports · 2020Review
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
BACKGROUND Transforming growth factor (TGF)-β1 is involved in the pathogenesis of coronary artery disease (CAD), but the mechanism of its action remains unclear. Our study aimed to investigate the role of TGF-β1 in CAD and to explore the possible mechanisms. MATERIAL AND METHODS A total of 60 CAD patients and 54 healthy people were included in this study. Blood samples were drawn from each participant to prepare serum. ELISA was utilized to measure serum level of TGF-β1. TGF-β1 expression vector, TGF-β1 siRNA, and TIMP-1 siRNA were transfected into human primary coronary artery endothelial cell (HCAEC) line cells, and expression of TGF-β1 sphingosine kinase 1 (SPHK1) and TIMP metallopeptidase inhibitor 1 (TIMP-1) was detected by Western blot. Cell apoptosis was detected by MTT assay. RESULTS Serum level of TGF-β1 was specifically higher in patients with CAD than in healthy controls. Serum levels of active TGF-β1 can be used to effectively distinguish CAD patients from healthy controls. TGF-β1 overexpression promoted the apoptosis of HCAEC and TGF-β1 siRNA silencing inhibited the apoptosis of HCAEC. TGF-β1 overexpression also promoted the expression of SPHK1 and TIMP-1. SPHK1 overexpression upregulated TIMP-1 but it showed no significant effects on TGF-β1. TIMP-1 overexpression showed no significant effects on TGF-β1 or SPHK1. SPHK1 inhibitor and TIMP-1 silencing reduced the enhancing effects of TGF-β1 overexpression on cell apoptosis. CONCLUSIONS TGF-β1 appears to promote CAD through the induction of cell apoptosis by upregulating SPHK1 expression and further upregulating its downstream TIMP-1.
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