Evidence map›Paper›PMID 26709517›Full record

ArticlePloS one2015

Phosphodiesterase 5a Inhibition with Adenoviral Short Hairpin RNA Benefits Infarcted Heart Partially through Activation of Akt Signaling Pathway and Reduction of Inflammatory Cytokines.

Longhu Li, Dong Zhao, Zhe Jin, Jian Zhang, Christian Paul, Yigang Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 5 institutions in 2 countries.

Longhu LiDepartment of Cardiology, the First Hospital of Qiqihaer City, Qiqihaer, China.
Dong ZhaoCollaborative Innovation Center of Judicial Civilization, China, Key Laboratory of Evidence Science (China University of Political Science and Law), Ministry of Education, Beijing, China.
Zhe JinDepartment of Cardiology, the First Hospital of Qiqihaer City, Qiqihaer, China.
Jian ZhangDepartment of EICU, the Affiliated Zhongshan Hospital of Dalian University, Dalian, China.
Christian PaulDepartment of Pathology and Lab Medicine, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, Ohio, 45267, United States of America.
Yigang WangDepartment of Pathology and Lab Medicine, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, Ohio, 45267, United States of America.
Qiqihar Medical University · CNAffiliated Zhongshan Hospital of Dalian University · CNChina University of Political Science and Law · CNSabin Vaccine Institute · USUniversity of Cincinnati Medical Center · US

Funding

Angiomyogenesis With Myoblast Derived iPS CellsR01HL107957 · NHLBI · UNIVERSITY OF CINCINNATI · PI WANG, YIGANG · 2011 to 2015
$3.4M
iPS cells-derived progenitor cells for angiomyogenesisR01HL110740 · NHLBI · UNIVERSITY OF CINCINNATI · PI ASHRAF, MUHAMMAD, WANG, YIGANG · 2011 to 2015
$2.9M
NHLBI NIH HHS HL-107957NHLBI NIH HHS HL-110740NHLBI NIH HHS R01 HL107957NHLBI NIH HHS R01 HL110740
6 · The paper itself

Abstract

introductionTreatment with short hairpin RNA (shRNA) interference therapy targeting phosphodiesterase 5a after myocardial infarction (MI) has been shown to mitigate post-MI heart failure. We investigated the mechanisms that underpin the beneficial effects of PDE5a inhibition through shRNA on post-MI heart failure.

methodsAn adenoviral vector with an shRNA sequence inserted was adopted for the inhibition of phosphodiesterase 5a (Ad-shPDE5a) in vivo and in vitro. Myocardial infarction (MI) was induced in male C57BL/6J mice by left coronary artery ligation, and immediately after that, the Ad-shPDE5a was injected intramyocardially around the MI region and border areas.

resultsFour weeks post-MI, the Ad-shPDE5a-treated mice showed significant mitigation of the left ventricular (LV) dilatation and dysfunction compared to control mice. Infarction size and fibrosis were also significantly reduced in Ad-shPDE5a-treated mice. Additionally, Ad-shPDE5a treatment decreased the MI-induced inflammatory cytokines interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and transforming growth factor-β1, which was confirmed in vitro in Ad-shPDE5a transfected myofibroblasts cultured under oxygen glucose deprivation. Finally, Ad-shPDE5a treatment was found to activate the myocardial Akt signaling pathway in both in vivo and in vitro experiments.

conclusionThese findings indicate that PDE5a inhibition by Ad-shPDE5a via the Akt signal pathway could be of significant value in the design of future therapeutics for post-MI heart failure.

Indexed as

AnimalsCells, CulturedCyclic Nucleotide Phosphodiesterases, Type 5CytokinesDisease Models, AnimalHeart FailureInflammation MediatorsMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardiumMyofibroblastsPhosphodiesterase 5 InhibitorsProto-Oncogene Proteins c-aktRNA, Small InterferingCyclic Nucleotide Phosphodiesterases, Type 5CytokinesInflammation MediatorsPde5a protein, mousePhosphodiesterase 5 InhibitorsProto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID26709517
PMCPMC4692549
OpenAlexW2256286019

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.