ArticleFrontiers in pharmacology2018
Luteolin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting TGFBR1 Signaling.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
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- Quality Control of Shenqi Tongmai Oral Liquid Based on Quantitative Analysis of Multicomponents by Single Marker, Molecular Docking, and Multivariate Statistics.Phytochemical analysis : PCA · 2025Article
- Luteolin: a natural product with multiple mechanisms for atherosclerosis.Frontiers in pharmacology · 2025Review
- Mechanism of Artemisia annua L. in the treatment of acute myocardial infarction: network pharmacology, molecular docking and in vivo validation.Molecular diversity · 2024Article
- Luteolin enhances drug chemosensitivity by downregulating the FAK/PI3K/AKT pathway in paclitaxel‑resistant esophageal squamous cell carcinoma.International journal of molecular medicine · 2024Article
- Citropten Inhibits Vascular Smooth Muscle Cell Proliferation and Migration via the TRPV1 Receptor.ACS omega · 2024Article
- MicroRNA-30a-3p: a potential noncoding RNA target for the treatment of arteriosclerosis obliterans.Aging · 2023Article
- Bioflavonoid luteolin prevents sFlt-1 release via HIF-1α inhibition in cultured human placenta.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Immunopharmacological Activities of Luteolin in Chronic Diseases.International journal of molecular sciences · 2023Review
- Hexahydrocurcumin mitigates angiotensin II-induced proliferation, migration, and inflammation in vascular smooth muscle cells.EXCLI journal · 2023Article
- IL-1β promotes A7r5 and HASMC migration and invasion via the p38-MAPK/Angpt-2 pathway.European journal of medical research · 2022Article
- Ginsenoside Rh1 Inhibits Angiotensin II-Induced Vascular Smooth Muscle Cell Migration and Proliferation through Suppression of the ROS-Mediated ERK1/2/p90RSK/KLF4 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- Through network pharmacology and molecular docking to explore the underlying mechanism ofFrontiers in physiology · 2022Article
- Ginsenoside Ro, an oleanolic saponin ofJournal of ginseng research · 2022Article
- Natural Flavonoids Derived From Fruits Are Potential Agents Against Atherosclerosis.Frontiers in nutrition · 2022Review
- Pregestational diabetes alters cardiac structure and function of neonatal rats through developmental plasticity.Frontiers in cardiovascular medicine · 2022Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cell (VSMC) proliferation and migration play a critical role in the development of arterial remodeling during various vascular diseases including atherosclerosis, hypertension, and related diseases. Luteolin is a food-derived flavonoid that exerts protective effects on cardiovascular diseases. Here, we investigated whether transforming growth factor-β receptor 1 (TGFBR1) signaling underlies the inhibitory effects of luteolin on VSMC proliferation and migration. We found that luteolin reduced the proliferation and migration of VSMCs, specifically A7r5 and HASMC cells, in a dose-dependent manner, based on MTS and EdU, and Transwell and wound healing assays, respectively. We also demonstrated that it inhibited the expression of proliferation-related proteins including PCNA and Cyclin D1, as well as the migration-related proteins MMP2 and MMP9, in a dose-dependent manner by western blotting. In addition, luteolin dose-dependently inhibited the phosphorylation of TGFBR1, Smad2, and Smad3. Notably, adenovirus-mediated overexpression of TGFBR1 enhanced TGFBR1, Smad2, and Smad3 activation in VSMCs and partially blocked the inhibitory effect of luteolin on TGFBR1, Smad2, and Smad3. Moreover, overexpression of TGFBR1 rescued the inhibitory effects of luteolin on the proliferation and migration of VSMCs. Additionally, molecular docking showed that this compound could dock onto an agonist binding site of TGFBR1, and that the binding energy between luteolin and TGFBR1 was -10.194 kcal/mol. Simulations of molecular dynamics showed that TGFBR1-luteolin binding was stable. Collectively, these data demonstrated that luteolin might inhibit VSMC proliferation and migration by suppressing TGFBR1 signaling.
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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.