Evidence map›Paper›PMID 26833319›Full record

SynthesisHeart failure reviews2016

Pathophysiological mechanism and therapeutic role of S100 proteins in cardiac failure: a systematic review.

Egidio Imbalzano, Giuseppe Mandraffino, Marco Casciaro, Sebastiano Quartuccio, Antonino Saitta, Sebastiano Gangemi

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023
    Review
  6. Article
  7. Review
  8. Alarmins, COVID-19 and comorbidities.Annals of medicine · 2021
    Review
  9. Article
  10. Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021
    Review
  11. Article
  12. IL-33 in Mental Disorders.Medicina (Kaunas, Lithuania) · 2021
    Review
  13. Article
  14. Commentary: Doubling down on adeno-associated viruses for cardiac gene therapy.The Journal of thoracic and cardiovascular surgery · 2020
    Article
  15. Article
  16. Article
  17. Observational
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Egidio ImbalzanoDepartment of Clinical and Experimental Medicine, Policlinic University of Messina, Via Consolare Valeria n.1, 98125, Messina, Italy. eimbalzano@unime.it.
Giuseppe MandraffinoDepartment of Clinical and Experimental Medicine, Policlinic University of Messina, Via Consolare Valeria n.1, 98125, Messina, Italy.
Marco CasciaroSchool and Division of Allergy and Clinical Immunology, University of Messina, Messina, Italy.
Sebastiano QuartuccioDepartment of Clinical and Experimental Medicine, Policlinic University of Messina, Via Consolare Valeria n.1, 98125, Messina, Italy.
Antonino SaittaDepartment of Clinical and Experimental Medicine, Policlinic University of Messina, Via Consolare Valeria n.1, 98125, Messina, Italy.
Sebastiano GangemiSchool and Division of Allergy and Clinical Immunology, University of Messina, Messina, Italy.
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

S100 proteins are a family of highly acidic calcium-binding proteins involved in calcium handling in many tissues and organs. Some of these proteins are highly expressed in cardiac tissue, and an impairment of some specific S100 proteins has been related to heart failure. To check this hypothesis, we decided to review the literature since 2008 until May 2015. According to the studies collected, recovering S100A1 levels may enhance contractile/relaxing performance in heart failure, reverse negative force-frequency relationship, improve contractile reserve, reverse diastolic dysfunction and protect against pro-arrhythmic reductions of sarcoplasmic reticulum calcium. The safety profile of gene therapy was also confirmed. Increased S100B protein levels were related to a worse outcome in chronic heart failure. S100A8/A9 complex plasma levels, as well as other inflammatory biomarkers, were significantly higher in chronic heart failure patients. S100A2 seems to increase both contractile and relaxation performance in animal cardiomyocytes. Otherwise, S100A6 cardiac expression seems to have no effects on contractility. S100A4 KO mice showed reduced cardiac interstitial fibrosis. Data collected encourage a potential prospective application in human. These proteins could be exploited as biomarkers in stadiation and prognosis of chronic heart failure, as well as therapeutic target to rescue failing heart. Registration details The study protocol has been registered in PROSPERO ( http://www.crd.york.ac.uk/PROSPERO/ ) under registration number CRD42015027932.

Indexed as

Genetic TherapyAnimalsCalciumDisease Models, AnimalGene TargetingHeart FailureHumansMiceS100 ProteinsCalciumS100 ProteinsAlarminsBiomarkersGene therapyHeart failureS100A1S100 proteinsSystematic review

Identifiers

PMID26833319
OpenAlexW2298209933

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.