ArticleInternational journal of clinical and experimental pathology2015
Apigenin inhibits TGF-β1-induced proliferation and migration of airway smooth muscle cells.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Integrative bioinformatics and machine learning to explore the mechanism of Scutellaria baicalensis Georgi in TGF-β1-induced ASMCs proliferation during asthma airway remodeling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway.Frontiers in genetics · 2026Article
- The Antioxidative Effects of Flavones in Hypertensive Disease.Biomedicines · 2023Review
- Asthma and Chronic Rhinosinusitis: How Similar Are They in Pathogenesis and Treatment Responses?International journal of molecular sciences · 2021Review
- Let-7a inhibits proliferation and promotes apoptosis of human asthmatic airway smooth muscle cells.Experimental and therapeutic medicine · 2019Article
- Crosstalk Between Signaling Pathways Involved in the Regulation of Airway Smooth Muscle Cell Hyperplasia.Frontiers in pharmacology · 2019Review
- Apigenin attenuates PM2.5-induced airway hyperresponsiveness and inflammation by down-regulating NF-κB in murine model of asthma.International journal of clinical and experimental pathology · 2019Article
- Transforming growth factor-β1 up-regulates connexin43 expression in osteocytes via canonical Smad-dependent signaling pathway.Bioscience reports · 2018Article
- Apigenin alleviates TGF-β1-induced nasal mucosa remodeling by inhibiting MAPK / NF-kB signaling pathways in chronic rhinosinusitis.PloS one · 2018Article
- Apigenin inhibits renal cell carcinoma cell proliferation.Oncotarget · 2017Article
- [Inhibitory effect of KyoT2 overexpression on proliferation and migration of airway smooth muscle cells in mice with asthma].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that the proliferation and migration of ASM cells (ASMCs) plays an important role in the pathogenesis of airway remodeling in asthma. Previous studies reported that apigenin can inhibit airway remodeling in a mouse asthma model. However, its effects on the proliferation and migration of ASMCs in asthma remain unknown. Therefore, the aim of our present study was to investigate the effects of apigenin on ASMC proliferation and migration, and explore the possible molecular mechanism. We found that apigenin inhibited transforming growth factor-β1 (TGF-β1)-induced ASMC proliferation. The cell cycle was blocked at G1/S-interphase by apigenin. It also suppressed TGF-β1-induced ASMCs migration. Furthermore, apigenin inhibited TGF-β1-induced Smad 2 and Smad 3 phosphorylation in ASMCs. Taken together, these results suggested that apigenin inhibited the proliferation and migration of TGF-β1-stimulated ASMCs by inhibiting Smad signaling pathway. These data might provide useful information for treating asthma and show that apigenin has potential for attenuating airway remodeling.
Indexed as
Identifiers
26722444PMC4680389W2418065255What 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.