Evidence map›Paper›PMID 29392537›Full record

ArticleJournal of cardiovascular translational research2018

Enhanced Cardiac S100A1 Expression Improves Recovery from Global Ischemia-Reperfusion Injury.

S Jungi, X Fu, A Segiser, M Busch, P Most, M Fiedler, T Carrel, H Tevaearai Stahel, S L Longnus, Henriette Most

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 2018. 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
1.2field-weighted citation impact, top 23% 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, 11 citations in OpenAlex.

  1. Translational cancer research · 2024
    Article
  2. Calcium signaling in mitochondrial intermembrane space.Biochemical Society transactions · 2024
    Review
  3. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
  4. Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Observational
  9. Article
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

10 authors at 2 institutions in 2 countries.

S JungiDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
X FuDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
A SegiserDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
M BuschSection for Molecular and Translational Cardiology, Department of Cardiology, Pneumology and Angiology, Karl-Ruprechts University of Heidelberg, Heidelberg, Germany.
P MostSection for Molecular and Translational Cardiology, Department of Cardiology, Pneumology and Angiology, Karl-Ruprechts University of Heidelberg, Heidelberg, Germany.
M FiedlerCenter for Laboratory Medicine, Inselspital University Hospital, University of Bern, Bern, Switzerland.
T CarrelDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
H Tevaearai StahelDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
S L LongnusDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland.
Henriette MostDepartment of Cardiovascular Surgery, Inselspital University Hospital, University of Bern, 3010, Bern, Switzerland. henriette.most@insel.ch.ORCID 0000-0002-8970-1318
University of Bern · CHHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene-targeted therapy with the inotropic Ca2 + -sensor protein S100A1 rescues contractile function in post-ischemic heart failure and is being developed towards clinical trials. Its proven beneficial effect on cardiac metabolism and mitochondrial function suggests a cardioprotective effect of S100A1 in myocardial ischemia-reperfusion injury (IRI). Fivefold cardiomyocyte-specific S100A1 overexpressing, isolated rat hearts perfused in working mode were subjected to 28 min ischemia (37 °C) followed by 60 min reperfusion. S100A1 overexpressing hearts showed superior hemodynamic recover: Left ventricular pressure recovered to 57 ± 7.3% of baseline compared to 51 ± 4.6% in control (p = 0.025), this effect mirrored in LV work and dP/dt(max). Troponin T and lactate dehydrogenase was decreased in the S100A1 group, as well as FoxO pro-apoptotic transcription factor, indicating less tissue necrosis, whereas phosphocreatine content was higher after reperfusion. This is the first report of a cardioprotective effect of S100A1 overexpression in a global IRI model.

Indexed as

Myocardial ContractionVentricular Function, LeftAnimalsDependovirusDisease Models, AnimalGenetic TherapyGenetic VectorsGene Transfer TechniquesHumansIsolated Heart PreparationMaleMyocardial Reperfusion InjuryMyocardiumRats, Inbred LewRecovery of FunctionS100 ProteinsS100A1 proteinS100 ProteinsCardioprotectionInotropic therapyIschemia-reperfusion injuryS100A1

Identifiers

PMID29392537
OpenAlexW2792895404

What OpenQuestion holds

Textmetadata
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.