Evidence map›Paper›PMID 25014216›Full record

ArticlePloS one2014

PARP-inhibitor treatment prevents hypertension induced cardiac remodeling by favorable modulation of heat shock proteins, Akt-1/GSK-3β and several PKC isoforms.

Laszlo Deres, Eva Bartha, Anita Palfi, Krisztian Eros, Adam Riba, Janos Lantos, Tamas Kalai, Kalman Hideg, Balazs Sumegi, Ferenc Gallyas and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 38 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

12 authors at 1 institution in 1 country.

Laszlo DeresFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary; Szentagothai Janos Research Center, University of Pécs, Medical School, Pécs, Hungary.
Eva BarthaFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary.
Anita PalfiFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary.
Krisztian ErosFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary; Szentagothai Janos Research Center, University of Pécs, Medical School, Pécs, Hungary.
Adam RibaFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary; Szentagothai Janos Research Center, University of Pécs, Medical School, Pécs, Hungary.
Janos LantosDepartment of Surgical Research and Techniques, University of Pécs, Pécs, Hungary.
Tamas KalaiDepartment of Organic and Medicinal Chemistry, University of Pécs, Pécs, Hungary.
Kalman HidegDepartment of Organic and Medicinal Chemistry, University of Pécs, Pécs, Hungary.
Balazs SumegiSzentagothai Janos Research Center, University of Pécs, Medical School, Pécs, Hungary; Department of Biochemistry and Medical Chemistry, Medical School, University of Pécs, Pécs, Hungary; MTA-PTE Nuclear-Mitochondrial Interactions Research Group, Pécs, Hungary.
Ferenc GallyasDepartment of Biochemistry and Medical Chemistry, Medical School, University of Pécs, Pécs, Hungary; MTA-PTE Nuclear-Mitochondrial Interactions Research Group, Pécs, Hungary.
Kalman TothFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary.
Robert HalmosiFirst Department of Medicine, Division of Cardiology, University of Pécs, Pécs, Hungary; Szentagothai Janos Research Center, University of Pécs, Medical School, Pécs, Hungary.
University of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneously hypertensive rat (SHR) is a suitable model for studies of the complications of hypertension. It is known that activation of poly(ADP-ribose) polymerase enzyme (PARP) plays an important role in the development of postinfarction as well as long-term hypertension induced heart failure. In this study, we examined whether PARP-inhibitor (L-2286) treatment could prevent the development of hypertensive cardiopathy in SHRs. 6-week-old SHR animals were treated with L-2286 (SHR-L group) or placebo (SHR-C group) for 24 weeks. Wistar-Kyoto rats were used as aged-matched, normotensive controls (WKY group). Echocardiography was performed, brain-derived natriuretic peptide (BNP) activity and blood pressure were determined at the end of the study. We detected the extent of fibrotic areas. The amount of heat-shock proteins (Hsps) and the phosphorylation state of Akt-1(Ser473), glycogen synthase kinase (GSK)-3β(Ser9), forkhead transcription factor (FKHR)(Ser256), mitogen activated protein kinases (MAPKs), and protein kinase C (PKC) isoenzymes were monitored. The elevated blood pressure in SHRs was not influenced by PARP-inhibitor treatment. Systolic left ventricular function and BNP activity did not differ among the three groups. L-2286 treatment decreased the marked left ventricular (LV) hypertrophy which was developed in SHRs. Interstitial collagen deposition was also decreased by L-2286 treatment. The phosphorylation of extracellular signal-regulated kinase (ERK)1/2(Thr183-Tyr185), Akt-1(Ser473), GSK-3β(Ser9), FKHR(Ser256), and PKC ε(Ser729) and the level of Hsp90 were increased, while the activity of PKC α/βII(Thr638/641), ζ/λ(410/403) were mitigated by L-2286 administration. We could detect signs of LV hypertrophy without congestive heart failure in SHR groups. This alteration was prevented by PARP inhibition. Our results suggest that PARP-inhibitor treatment has protective effect already in the early stage of hypertensive myocardial remodeling.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAnimalsBlood PressureExtracellular Signal-Regulated MAP KinasesForkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeart FailureHSP90 Heat-Shock ProteinsHypertensionHypertrophy, Left VentricularIsoenzymesMaleNatriuretic Peptide, Brain2-((2-piperidin-1-ylethyl)thio)quinazolin-4(3H)-oneAkt1 protein, ratExtracellular Signal-Regulated MAP KinasesForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, ratGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratHSP90 Heat-Shock ProteinsIsoenzymesNatriuretic Peptide, BrainNerve Tissue ProteinsPiperidinesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein Kinase CProto-Oncogene Proteins c-aktQuinazolines

Identifiers

PMID25014216
PMCPMC4094529
OpenAlexW2083751740

What OpenQuestion holds

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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.