ArticleActa Cardiologica Sinica2016
Aliskiren Inhibits Neointimal Matrix Metalloproteinases in Experimental Atherosclerosis.
Article in Acta Cardiologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 5 citations in OpenAlex.
- Cardiac Radiofrequency Ablation Exacerbates Myocardial Injury through Pro-Inflammatory Response and Pro-Oxidative Stress in Elderly Patients with Persistent Atrial Fibrillation.Current vascular pharmacology · 2024Article
- Renin-Angiotensin System in Pathogenesis of Atherosclerosis and Treatment of CVD.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe renin-angiotensin system (RAS) plays an important role in atherosclerosis. Acting via the angiotensin II receptor, type 1, oxidative stress increases and contributes to endothelial dysfunction and vascular inflammation. Renin exerts effects through a renin receptor causing an increase in the efficiency of angiotensinogen cleavage and facilitates angiotensin II (Ang II) generation and action on cell surfaces. Ang II enhances proliferation and migration of vascular smooth muscle cells, indicating a direct involvement of the RAS in smooth muscle cell proliferation during neointimal formation. Aliskiren, a direct renin inhibitor, is a new oral antihypertensive drug. However, the role of the direct renin inhibitor in neointimal formation and vascular matrix metalloproteinases remains unclear.
methodsTo investigate the effects of aliskiren on the expression of vascular matrix metalloproteinases, we evaluated the aortic neointimal formation of high-cholesterol-fed animals after vascular injury in vivo and the cellular function of the tumor necrosis factor-α stimulated human aortic smooth muscle cells in vitro. Thereafter, we evaluated vascular expression (by western blot), activity (by gelatin zymography) and molecular pathway.
resultsIn this study we demonstrated that aliskiren reduced neointimal hyperplasia in hypercholesterolemic rabbits after vascular injury and the expression of matrix metalloproteinases in the neointima. Aliskiren also inhibited the expression and activities of matrix metalloproteinases on tumor necrosis factor-α (TNF-α)-stimulated human aortic smooth muscle cells via the mitogen-activated protein kinase pathway.
conclusionsThe present study showed that aliskiren inhibited the expression of vascular matrix metalloproteinases. With these results, we have better clarified the potential role of renin inhibitors in human atherosclerosis.
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.