Evidence map›Paper›PMID 33142923›Full record

ArticleInternational journal of molecular sciences2020

Heme-Induced Oxidation of Cysteine Groups of Myofilament Proteins Leads to Contractile Dysfunction of Permeabilized Human Skeletal Muscle Fibres.

Gerardo Alvarado, Attila Tóth, Éva Csősz, Gergő Kalló, Katalin Dankó, Zoltán Csernátony, Ann Smith, Magnus Gram, Bo Akerström, István Édes and 3 more

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

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    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.

Gerardo AlvaradoHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, H-4032 Debrecen, Hungary.ORCID 0000-0002-1914-0260
Attila TóthHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, H-4032 Debrecen, Hungary.
Éva CsőszProteomics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.ORCID 0000-0003-4373-2175
Gergő KallóProteomics Core Facility, Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
Katalin DankóDepartment of Rheumatology, Institute of Internal Medicine, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
Zoltán CsernátonyDepartment of Orthopedics, Faculty of Medicine, University of Debrecen, H-4012 Debrecen, Hungary.
Ann SmithDepartment of Cell and Molecular Biology and Biochemistry, School of Biological and Chemical Sciences, University of Missouri-Kansas City, Missouri, MO 64110, USA.
Magnus GramDepartment of Clinical Sciences Lund, Pediatrics, Lund University, 22184 Lund, Sweden.ORCID 0000-0002-5880-2925
Bo AkerströmDepartment of Clinical Sciences Lund, Infection Medicine, Lund University, 22184 Lund, Sweden.
István ÉdesDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.
György BallaInstitute of Pediatrics, Faculty of Medicine, University of Debrecen, H-4012 Debrecen, Hungary.
Zoltán PappHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, H-4032 Debrecen, Hungary.
József BallaHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, H-4032 Debrecen, Hungary.
University of Debrecen · HULund University · SEUniversity of Missouri–Kansas City · US

Funding

Hungarian Scientific Research Fund GINOP-2.3.2-15-2016-00043 projectHungarian Scientific Research Fund K 109083Hungarian Scientific Research Fund K 84300Hungarian Scientific Research Fund OTKA-K112333
6 · The paper itself

Abstract

Heme released from red blood cells targets a number of cell components including the cytoskeleton. The purpose of the present study was to determine the impact of free heme (20-300 µM) on human skeletal muscle fibres made available during orthopedic surgery. Isometric force production and oxidative protein modifications were monitored in permeabilized skeletal muscle fibre segments. A single heme exposure (20 µM) to muscle fibres decreased Ca

Indexed as

Amino Acid SequenceCalciumCysteineHemeHumansMass SpectrometryMuscle ContractionMuscle Fibers, SkeletalMuscle ProteinsMyofibrilsOxidation-ReductionCalciumCysteineHemeMuscle Proteinschronic heart failurecontractile dysfunctionhemehemopexinoxidationskeletal muscle fibreskeletal muscle myopathysulfenic acid formationsulfhydryl groupsα1-microglobulin

Identifiers

PMID33142923
PMCPMC7663642
OpenAlexW3096733279

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.