Evidence map›Paper›PMID 32731559›Full record

ArticleMolecules (Basel, Switzerland)2020

Decorin Protects Cardiac Myocytes against Simulated Ischemia/Reperfusion Injury.

Renáta Gáspár, Kamilla Gömöri, Bernadett Kiss, Ágnes Szántai, János Pálóczi, Zoltán V Varga, Judit Pipis, Barnabás Váradi, Bence Ágg, Tamás Csont and 3 more

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

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. NormothermicStem cells international · 2022
    Article
  8. Article
  9. Review
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

13 authors at 3 institutions in 3 countries.

Renáta GáspárMetabolic Diseases and Cell Signaling (MEDICS) Research Group, Department of Biochemistry, Interdisciplinary Excellence Centre, University of Szeged, Dom ter 9, H-6720 Szeged, Hungary.
Kamilla GömöriCardiovascular Research Group, Department of Pharmacology and Pharmacotherapy, University of Szeged, Dom ter 12, H-6720 Szeged, Hungary.
Bernadett KissCardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, H-1089 Budapest, Hungary.
Ágnes SzántaiCardiovascular Research Group, Department of Pharmacology and Pharmacotherapy, University of Szeged, Dom ter 12, H-6720 Szeged, Hungary.
János PálócziCardiovascular Research Group, Department of Pharmacology and Pharmacotherapy, University of Szeged, Dom ter 12, H-6720 Szeged, Hungary.
Zoltán V VargaCardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, H-1089 Budapest, Hungary.
Judit PipisPharmahungary Group, Hajnoczy utca 6, H-6722 Szeged, Hungary.
Barnabás VáradiCardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, H-1089 Budapest, Hungary.
Bence ÁggCardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, H-1089 Budapest, Hungary.
Tamás CsontMetabolic Diseases and Cell Signaling (MEDICS) Research Group, Department of Biochemistry, Interdisciplinary Excellence Centre, University of Szeged, Dom ter 9, H-6720 Szeged, Hungary.
Péter FerdinandyCardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvarad ter 4, H-1089 Budapest, Hungary.ORCID 0000-0002-5210-5184
Monika BartekováInstitute for Heart Research, Centre of Experimental Medicine, Slovak Academy of Sciences, Dúbravská cesta 9, 841 04 Bratislava, Slovak.
Anikó GörbeCardiovascular Research Group, Department of Pharmacology and Pharmacotherapy, University of Szeged, Dom ter 12, H-6720 Szeged, Hungary.
Semmelweis University · HUUniversity of Szeged · HUSlovak Academy of Sciences · SK

Funding

Hungarian National Research, Development and Innovation Office Bolyai János fellowshipHungarian National Research, Development and Innovation Office GINOP-2.3.2-15-2016-00040Hungarian National Research, Development and Innovation Office NVKP_ 16-1-2016-0017Hungarian National Research, Development and Innovation Office OTKA PD 106001Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic and the Slovak Academy of Sciences VEGA no. 2/0104/20
6 · The paper itself

Abstract

Search for new cardioprotective therapies is of great importance since no cardioprotective drugs are available on the market. In line with this need, several natural biomolecules have been extensively tested for their potential cardioprotective effects. Previously, we have shown that biglycan, a member of a diverse group of small leucine-rich proteoglycans, enhanced the expression of cardioprotective genes and decreased ischemia/reperfusion-induced cardiomyocyte death via a TLR-4 dependent mechanism. Therefore, in the present study we aimed to test whether decorin, a small leucine-rich proteoglycan closely related to biglycan, could exert cardiocytoprotection and to reveal possible downstream signaling pathways. Methods: Primary cardiomyocytes isolated from neonatal and adult rat hearts were treated with 0 (Vehicle), 1, 3, 10, 30 and 100 nM decorin as 20 h pretreatment and maintained throughout simulated ischemia and reperfusion (SI/R). In separate experiments, to test the mechanism of decorin-induced cardio protection, 3 nM decorin was applied in combination with inhibitors of known survival pathways, that is, the NOS inhibitor L-NAME, the PKG inhibitor KT-5823 and the TLR-4 inhibitor TAK-242, respectively. mRNA expression changes were measured after SI/R injury. Results: Cell viability of both neonatal and adult cardiomyocytes was significantly decreased due to SI/R injury. Decorin at 1, 3 and 10 nM concentrations significantly increased the survival of both neonatal and adult myocytes after SI/R. At 3nM (the most pronounced protective concentration), it had no effect on apoptotic rate of neonatal cardiac myocytes. No one of the inhibitors of survival pathways (L-NAME, KT-5823, TAK-242) influenced the cardiocytoprotective effect of decorin. MYND-type containing 19 (Zmynd19) and eukaryotic translation initiation factor 4E nuclear import factor 1 (Eif4enif1) were significantly upregulated due to the decorin treatment. In conclusion, this is the first demonstration that decorin exerts a direct cardiocytoprotective effect possibly independent of NO-cGMP-PKG and TLR-4 dependent survival signaling.

Indexed as

AnimalsCardiotonic AgentsCell SurvivalDecorinMyocardial Reperfusion InjuryMyocytes, CardiacRatsRats, WistarSignal TransductionCardiotonic AgentsDcn protein, ratDecorincardiac myocytescardio protectiondecorinischemia/reperfusion injuryproteoglycan

Identifiers

PMID32731559
PMCPMC7436189
OpenAlexW3046126721

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.