Evidence map›Paper›PMID 31123275›Full record

ArticleScientific reports2019

Sildenafil Reduces Neointimal Hyperplasia after Angioplasty and Inhibits Platelet Aggregation via Activation of cGMP-dependent Protein Kinase.

Han-Mo Yang, Sooryeonhwa Jin, Hyunduk Jang, Ju-Young Kim, Joo-Eun Lee, Joonoh Kim, Hyo-Soo Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  14. Targeting the SARS-CoV-2 3CLFuture cardiology · 2021
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  20. COVID-19 and Phosphodiesterase Enzyme Type 5 Inhibitors.Journal of microscopy and ultrastructure
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Han-Mo YangNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Sooryeonhwa JinNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Hyunduk JangNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Ju-Young KimNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Joo-Eun LeeNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Joonoh KimNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea.
Hyo-Soo KimNational Leading Laboratory for Stem Cell Research, Seoul National University College of Medicine, Seoul, Korea. hyosoo@snu.ac.kr.ORCID http://orcid.org/0000-0003-0847-5329
Seoul National University · KRSeoul National University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sildenafil is known to reduce cardiac hypertrophy through cGMP-dependent protein kinase (cGK) activation. Studies have demonstrated that cGK has a central switching role in modulating vascular smooth muscle cell (VSMC) phenotype in response to vascular injury. Here, we aimed to examine the effects of cGK activation by sildenafil on neointimal formation and platelet aggregation. After vascular injury, neointimal hyperplasia in rat carotid arteries was significantly reduced in the sildenafil-treated group. This effect of sildenafil was accompanied by the reduction of viability and migration of VSMCs. Further experiments showed that the increased cGK activity by sildenafil inhibited platelet-derived growth factor-induced phenotype change of VSMCs from a contractile form to a synthetic one. Conversely, the use of cGK inhibitor or gene transfer of dominant-negative cGK reversed the effects of sildenafil, increasing viability of VSMCs and neointimal formation. Interestingly, sildenafil significantly inhibited platelet aggregation induced by ADP or thrombin. This effect was reversed by cGK inhibitor, suggesting that sildenafil inhibits platelet aggregation via cGK pathway. This study demonstrated that sildenafil inhibited neointimal formation and platelet aggregation via cGK pathway. These results suggest that sildenafil could be a promising candidate for drug-eluting stents for the prevention of both restenosis and stent thrombosis.

Indexed as

AngioplastyAnimalsCell MovementCell ProliferationCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 5Muscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaPlatelet AggregationRatsSignal TransductionSildenafil CitrateVascular System InjuriesCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 5Sildenafil Citrate

Identifiers

PMID31123275
PMCPMC6533301
OpenAlexW2945684261

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.