ArticleDisease markers2014
Fluvastatin upregulates the α 1C subunit of CaV1.2 channel expression in vascular smooth muscle cells via RhoA and ERK/p38 MAPK pathways.
Article in Disease markers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Mechanisms of nebivolol-mediated effects on bFGF-induced vascular smooth muscle cell proliferation and migration.Current research in pharmacology and drug discovery · 2025Article
- Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways.The Journal of international medical research · 2024Article
- Corrigendum to "Fluvastatin Upregulates theDisease markers · 2024Article
- Elevated serum fatty acid-binding protein 4 level predicts all-cause and cardiovascular mortality in peritoneal dialysis patients: a five-year study.Renal failure · 2023Observational
- A heparin-rosuvastatin-loaded P(LLA-CL) nanofiber-covered stent inhibits inflammatory smooth-muscle cell viability to reduce in-stent stenosis and thrombosis.Journal of nanobiotechnology · 2021Article
- LncRNA H19/Runx2 axis promotes VSMCs transition via MAPK pathway.American journal of translational research · 2020Article
- Role of the Balance of Akt and MAPK Pathways in the Exercise-Regulated Phenotype Switching in Spontaneously Hypertensive Rats.International journal of molecular sciences · 2019Article
- CPT1 regulates the proliferation of pulmonary artery smooth muscle cells through the AMPK-p53-p21 pathway in pulmonary arterial hypertension.Molecular and cellular biochemistry · 2019Article
- Effects of paclitaxel intervention on pulmonary vascular remodeling in rats with pulmonary hypertension.Experimental and therapeutic medicine · 2019Article
- Crocin prevents platelet‑derived growth factor BB‑induced vascular smooth muscle cells proliferation and phenotypic switch.Molecular medicine reports · 2018Article
- Serum Amyloid A Induces a Vascular Smooth Muscle Cell Phenotype Switch through the p38 MAPK Signaling Pathway.BioMed research international · 2017Article
- Associations of Variants in the CACNA1A and CACNA1C Genes With Longitudinal Blood Pressure Changes and Hypertension Incidence: The GenSalt Study.American journal of hypertension · 2016Article
- Sustained Contraction in Vascular Smooth Muscle by Activation of L-type CaFrontiers in pharmacology · 2016Article
- Recent advance in treatment of atherosclerosis: Key targets and plaque-positioned delivery strategies.Journal of tissue engineeringReview
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal phenotypic switch of vascular smooth muscle cell (VSMC) is a hallmark of vascular disorders such as atherosclerosis and restenosis. And this process has been related to remodeling of L-type calcium channel (LTCC). We attempted to investigate whether fluvastatin has any effect on VSMC proliferation and LTCCα 1C subunit (LTCCα 1C) expression as well as the potential mechanisms involved. The VSMCs proliferation was assayed by osteopontin immunofluorescent staining and [(3)H]-thymidine incorporation. The cell cycle was detected by flow cytometric analysis. The activity of RhoA was determined with pull-down assay. MAPK activity and LTCCα 1C expression were assessed by western blotting. We demonstrated fluvastatin prevented the VSMCs dedifferentiating into a proliferative phenotype and induced cell cycle arrest in the G0/G1 phase in response to PDGF-BB stimulation. Fluvastatin dose-dependently reversed the downregulation of LTCCα 1C expression induced by PDGF-BB. Inhibition of ROCK, ERK, or p38 MAPK activation largely enhanced the upregulation effect of fluvastatin (P < 0.01). However, blockade of JNK pathway had no effect on LTCCα 1C expression. We concluded LTCCα 1C was a VSMC contractile phenotype marker gene. Fluvastatin upregulated LTCCα 1C expression, at least in part, by inhibiting ROCK, ERK1/2, and p38 MAPK activation. Fluvastatin may be a potential candidate for preventing or treating vascular diseases.
Indexed as
Identifiers
What 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.