Evidence map›Paper›PMID 28174168›Full record

ArticleJournal of the American Heart Association2017

Cardiac Overexpression of S100A6 Attenuates Cardiomyocyte Apoptosis and Reduces Infarct Size After Myocardial Ischemia-Reperfusion.

Azadeh Mofid, Nadav S Newman, Paul J H Lee, Cynthia Abbasi, Pratiek N Matkar, Dmitriy Rudenko, Michael A Kuliszewski, Hao H Chen, Kolsoom Afrasiabi, James N Tsoporis and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Cardiac gene delivery using ultrasound: State of the field.Molecular therapy. Methods & clinical development · 2024
    Review
  6. Review
  7. Article
  8. Single-cell analysis reveals lysyl oxidase (Lox)Journal of advanced research · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
  13. Apoptotic Cell Death in Bicuspid-Aortic-Valve-Associated Aortopathy.International journal of molecular sciences · 2023
    Article
  14. Article
  15. Article
  16. S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021
    Review
  20. 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

14 authors at 2 institutions in 1 country.

Azadeh MofidDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Nadav S NewmanDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Paul J H LeeDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Cynthia AbbasiDepartment of Physiology, University of Toronto, Ontario, Canada.
Pratiek N MatkarDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Dmitriy RudenkoDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Michael A KuliszewskiDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Hao H ChenDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Kolsoom AfrasiabiDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
James N TsoporisDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Anthony O GramoliniDepartment of Physiology, University of Toronto, Ontario, Canada.
Kim A ConnellyDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Thomas G ParkerDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada.
Howard Leong-PoiDivision of Cardiology, Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Ontario, Canada leong-poih@smh.ca.
St. Michael's Hospital · CAUniversity of Toronto · CA

Funding

CIHR MOP 137109CIHR MOP 62763
6 · The paper itself

Abstract

backgroundCardiomyocyte-specific transgenic mice overexpressing S100A6, a member of the family of EF-hand calcium-binding proteins, develop less cardiac hypertrophy, interstitial fibrosis, and myocyte apoptosis after permanent coronary ligation, findings that support S100A6 as a potential therapeutic target after acute myocardial infarction. Our purpose was to investigate S100A6 gene therapy for acute myocardial ischemia-reperfusion. METHODS AND

resultsWe first performed in vitro studies to examine the effects of S100A6 overexpression and knockdown in rat neonatal cardiomyocytes. S100A6 overexpression improved calcium transients and protected against apoptosis induced by hypoxia-reoxygenation via enhanced calcineurin activity, whereas knockdown of S100A6 had detrimental effects. For in vivo studies, human S100A6 plasmid or empty plasmid was delivered to the left ventricular myocardium by ultrasound-targeted microbubble destruction in Fischer-344 rats 2 days prior to a 30-minute ligation of the left anterior descending coronary artery followed by reperfusion. Control animals received no therapy. Pretreatment with S100A6 gene therapy yielded a survival advantage compared to empty-plasmid and nontreated controls. S100A6-pretreated animals had reduced infarct size and improved left ventricular systolic function, with less myocyte apoptosis, attenuated cardiac hypertrophy, and less cardiac fibrosis.

conclusionsS100A6 overexpression by ultrasound-targeted microbubble destruction helps ameliorate myocardial ischemia-reperfusion, resulting in lower mortality and improved left ventricular systolic function post-ischemia-reperfusion via attenuation of apoptosis, reduction in cardiac hypertrophy, and reduced infarct size. Our results indicate that S100A6 is a potential therapeutic target for acute myocardial infarction.

Indexed as

ApoptosisGene Expression Regulation, DevelopmentalAnimalsAnimals, NewbornBlotting, WesternCell Cycle ProteinsDisease Models, AnimalImmunohistochemistryIn Situ Nick-End LabelingMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacRatsRats, Inbred F344Real-Time Polymerase Chain ReactionRNACell Cycle ProteinsRNAS100a6 protein, ratS100 Calcium Binding Protein A6apoptosisgene therapyhypertrophyischemia‐reperfusionS100A6ultrasound‐targeted microbubble destruction

Identifiers

PMID28174168
PMCPMC5523770
OpenAlexW2587512795

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.