ArticleClinical and experimental pharmacology & physiology2020
Curcumin attenuates endothelial cell fibrosis through inhibiting endothelial-interstitial transformation.
Article in Clinical and experimental pharmacology & physiology, 2020. 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, 22 citations in OpenAlex.
- Antifibrotic mechanism of curcumin and its therapeutic potential in multi-organ diseases.Frontiers in pharmacology · 2026Review
- Curcumin protects the diabetic mouse retina by modulating the Hippo-YAP signaling pathway.International journal of ophthalmology · 2026Article
- Endothelial-to-Mesenchymal Transition in Health and Disease: Molecular Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Review
- Advances in Nanocarrier Systems for Overcoming Formulation Challenges of Curcumin: Current Insights.Nanomaterials (Basel, Switzerland) · 2024Review
- Review of the Protective Mechanism of Curcumin on Cardiovascular Disease.Drug design, development and therapy · 2024Review
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Benefits of Curcumin in the Vasculature: A Therapeutic Candidate for Vascular Remodeling in Arterial Hypertension and Pulmonary Arterial Hypertension?Frontiers in physiology · 2022Review
- Biomedical Applications and Bioavailability of Curcumin-An Updated Overview.Pharmaceutics · 2021Review
- Curcumin attenuates endothelial cell fibrosis through inhibiting endothelial-interstitial transformation.Clinical and experimental pharmacology & physiology · 2020Article
- The Evolving Role of Natural Compounds in the Medical Treatment of Uterine Fibroids.Journal of clinical medicine · 2020Review
- Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review.Frontiers in pharmacology · 2020Review
- Nanocurcumin: A Promising Candidate for Therapeutic Applications.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Curcumin (Cur) has various pharmacological activities, including anti-inflammatory, antiapoptotic and anticancer effects. However, there is no report on the effect of Cur on endothelial cell fibrosis. This study was designed to investigate the effect and mechanism of Cur on endothelial cell fibrosis. An endothelial cell fibrosis model was established by using transforming growth factor (TGF) induction. Proliferation assays, qRT-PCR, western blotting and immunostaining were performed to investigate the effects and mechanism of Cur on endothelial cell fibrosis. We found that in human umbilical vein endothelial cells (HUVECs), TGF-β1 treatment significantly decreased the expression of nuclear factor erythroid-2-related factor 2 (NRF-2), dimethylarginine dimethylaminohydrolase-1 (DDAH1), and VE-cadherin, the secretion of cellular nitric oxide (NO) and the activity of nitrous oxide synthase (NOS), while asymmetric dimethylarginine (ADMA) and the release of inflammatory factors were elevated. Immunofluorescence showed decreased CD31 and increased α-smooth muscle actin (α-SMA). Overexpression of NRF-2 significantly attenuated the effects of TGF-β1, while downregulation of DDAH1 potently counteracted the effect of NRF-2. In addition, ADMA treatment resulted in similar results to those of TGF-β1, and Cur significantly attenuated the effect of TGF-β1, accompanied by increased VE-cadherin, DDAH1 and NRF-2 and decreased matrix metalloproteinase-9 (MMP-9) and extracellular regulated protein kinases 1/2 (ERK1/2) phosphorylation. The NRF-2 inhibitor ML385 had the opposite effect as that of Cur. These results demonstrated that Cur inhibits TGF-β1-induced endothelial-to-mesenchymal transition (EndMT) by stimulating DDAH1 expression via the NRF-2 pathway, thus attenuating endothelial cell fibrosis.
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