ArticleInternational journal of clinical and experimental pathology2017
Decreased PPAR-γ expression after internal carotid artery stenting is associated with vascular lesions induced by smooth muscle cell proliferation and systemic inflammation in a minipig model.
Article in International journal of clinical and experimental pathology, 2017. 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
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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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Weighted Gene Co-Expression Network Analysis Reveals Key Genes and Potential Drugs in Abdominal Aortic Aneurysm.Biomedicines · 2021Article
- Targeting smooth muscle cell phenotypic switching in vascular disease.JVS-vascular science · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular restenosis after stenting is known to be largely mediated by proliferation of vascular smooth muscle cells. Recently, peroxisome proliferator-activated receptor gamma (PPAR-γ) has been implicated as a regulator of cellular inflammatory responses, and the PPAR-γ agonist rosiglitazone (ROSI) has been shown to attenuate atherosclerosis formation. However, whether ROSI can inhibit neointimal formation by regulating the inflammatory response and inhibiting vascular smooth muscle hyperplasia after stenting-induced injury remains to be clarified. Accordingly, in this study, 10 minipigs were randomly divided into two groups: the stenting group (n = 5) and the ROSI group (n = 5). Morphometric analysis was conducted for the stented arteries. The protein expressions of PPAR-γ and smooth muscle 22-alpha (SM22α) were analyzed by immunohistochemistry and western blotting, and the serum interferon-γ and interleukin-10 levels were measured by enzyme-linked immunosorbent assay. Three months after implantation, morphometric analysis revealed that administration of ROSI (0.5 mg/kg/d, continuous administration for 90 days) resulted in significant reductions of luminal stenosis, the neointimal area, and neointimal thickness, as compared to the stenting groups. The expression of PPAR-γ and the PPAR-γ/SM22α ratio in the ROSI group were higher than in the stenting group. Furthermore, the serum interferon-γ and interleukin-10 levels were found to be increased and to reach peak levels at 4 h and 7 days after stenting, respectively, after which both declined. However, ROSI treatment resulted in decreased interferon-γ and increased interleukin-10 levels after stenting. In both groups, the cytokine levels returned to the baseline levels on day 56 after stenting. Taken together, these results suggest that ROSI can reduce neointimal formation after stenting by inhibiting the local and systemic inflammatory responses as well as vascular smooth muscle hyperplasia.
Indexed as
Identifiers
31966579PMC6965304W3019269104What 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.