ArticleDrug design, development and therapy2018
Zoledronate inhibits fibroblasts' proliferation and activation via targeting TGF-β signaling pathway.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
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- Promising Adventitia in Atherosclerosis.Current vascular pharmacology · 2025Review
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- Anti‑metastatic activity of aromatic aminomethylidenebisphosphonates in a mouse model of 4T1 cell‑derived breast cancer.Oncology reports · 2023Article
- Candesartan treatment enhances liposome penetration and anti-tumor effect via depletion of tumor stroma and normalization of tumor vessel.Drug delivery and translational research · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious preclinical and clinical studies have demonstrated that zoledronate might inhibit neointimal hyperplasia at least partly by inhibiting the proliferation, adhesion and migration of vascular smooth muscle cells (VSMCs). However, whether zoledronate influences fibroblasts' proliferation and activation, which also play a key role in neointimal hyperplasia and vascular remodeling, remains largely unknown. In the present study, the effect of zoledronate on fibroblasts was investigated and the underlying molecular mechanisms were examined.
methodsAfter treatment with zoledronate, changes in biological behaviors, including the morphology, proliferation, cell-cycle distribution and migration of fibroblasts (NIH3T3 cells), were observed. The expression of α-SMA, TGF-β1 and TGF-β2 and the level of Smad2/3 phosphorylation in cultured fibroblasts were examined by Western blot. In vivo expression of α-SMA and TGF-β1 was assessed by immunohistochemical staining.
resultsIt was shown that the typical fibroblast cell morphology was altered after zoledronate exposure. Cultured fibroblasts treated with zoledronate displayed dose-dependent inhibition of cell proliferation due to cell-cycle arrest in the S phase. Cell migration activities were also dose dependently suppressed by zoledronate treatment. Expression of α-SMA in cultured fibroblasts was significantly reduced by zoledronate treatment. Further analysis showed decreased expression of TGF-β1 and α-SMA by periadventitial delivery of zoledronate in the rat carotid balloon-injury model. The expression of TGF-β1 and TGF-β2 and the phosphorylation of Smad2/3 in cultured fibroblasts were significantly inhibited by zoledronate treatment.
conclusionOur findings demonstrated that zoledronate can inhibit the proliferation, migration and activation of fibroblasts via the TGF-β signaling pathway and revealed a novel mechanism of zoledronate action against neointimal hyperplasia.
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