Evidence map›Paper›PMID 26881035›Full record

ReviewOxidative medicine and cellular longevity2016

Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology.

Alessia Arcaro, Flora Pirozzi, Annalisa Angelini, Cristina Chimenti, Lia Crotti, Carla Giordano, Daniele Mancardi, Daniele Torella, Carlo G Tocchetti

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. 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

9 authors at 8 institutions in 1 country.

Alessia ArcaroDepartment of Medicine and Health Sciences, University of Molise, 86100 Campobasso, Italy.
Flora PirozziDepartment of Translational Medical Sciences, Division of Internal Medicine, Federico II University, 80131 Naples, Italy.
Annalisa AngeliniCardiovascular Pathology Unit, Department of Thoracic, Cardiac and Vascular Sciences, University of Padova, 35121 Padova, Italy.
Cristina ChimentiLa Sapienza University and IRCCS L. Spallanzani, 00161 Rome, Italy.
Lia CrottiDepartment of Molecular Medicine, University of Pavia, 27100 Pavia, Italy; Center for Cardiac Arrhythmias of Genetic Origin, IRCCS Istituto Auxologico Italiano, 20135 Milano, Italy.
Carla GiordanoDepartment of Radiological, Oncological and Anatomo-Pathological Sciences, La Sapienza University, 00161 Rome, Italy.
Daniele MancardiDepartment of Clinical and Biological Sciences, University of Torino, 10043 Orbassano, Italy.
Daniele TorellaMolecular and Cellular Cardiology, Department of Medical and Surgical Sciences, Magna Graecia University, 88100 Catanzaro, Italy.
Carlo G TocchettiDepartment of Translational Medical Sciences, Division of Internal Medicine, Federico II University, 80131 Naples, Italy.
Federico II University Hospital · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITMagna Graecia University · ITSapienza University of Rome · ITUniversity of Molise · ITUniversity of Padua · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of heart failure (HF) is still increasing worldwide, with enormous human, social, and economic costs, in spite of huge efforts in understanding pathogenetic mechanisms and in developing effective therapies that have transformed this syndrome into a chronic disease. Myocardial redox imbalance is a hallmark of this syndrome, since excessive reactive oxygen and nitrogen species can behave as signaling molecules in the pathogenesis of hypertrophy and heart failure, leading to dysregulation of cellular calcium handling, of the contractile machinery, of myocardial energetics and metabolism, and of extracellular matrix deposition. Recently, following new interesting advances in understanding myocardial ROS and RNS signaling pathways, new promising therapeutical approaches with antioxidant properties are being developed, keeping in mind that scavenging ROS and RNS tout court is detrimental as well, since these molecules also play a role in physiological myocardial homeostasis.

Indexed as

Oxidation-ReductionAntioxidantsCalciumHeart FailureHomeostasisHumansItalyMitochondriaMyocardiumMyocytes, CardiacNitrogenOxidative StressPrognosisReactive Nitrogen SpeciesReactive Oxygen SpeciesSignal TransductionAntioxidantsCalciumNitrogenReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID26881035
PMCPMC4736421
OpenAlexW2222150581

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.