Evidence map›Paper›PMID 28648627›Full record

ArticleProgress in biophysics and molecular biology2017

Myofilament protein dynamics modulate EAD formation in human hypertrophic cardiomyopathy.

Melanie A Zile, Natalia A Trayanova

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

Article in Progress in biophysics and molecular biology, 2017. 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
1.1field-weighted citation impact, top 21% 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. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  8. Increased thin filament activation enhances alternans in human chronic atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  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

2 authors at 1 institution in 1 country.

Melanie A ZileInstitute for Computational Medicine and Department of Biomedical Engineering at Johns Hopkins University, 3400 N Charles St, 208 Hackerman Hall, Baltimore, MD 21218, USA. Electronic address: mzile@jhu.edu.
Natalia A TrayanovaInstitute for Computational Medicine and Department of Biomedical Engineering at Johns Hopkins University, 3400 N Charles St, 208 Hackerman Hall, Baltimore, MD 21218, USA. Electronic address: ntrayan1@jhu.edu.
Johns Hopkins University · US

Funding

Virtual Electrophysiology LaboratoryDP1HL123271 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TRAYANOVA, NATALIA A. · 2013 to 2017
$4.0M
Exploration of Arrhythmogenic Triggers and Substrates in Heart FailureR01HL126802 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI EFIMOV, IGOR R, GORELIK, JULIA · 2016 to 2019
$2.8M
NHLBI NIH HHS DP1 HL123271NHLBI NIH HHS R01 HL126802
6 · The paper itself

Abstract

Patients with hypertrophic cardiomyopathy (HCM), a disease associated with sarcomeric protein mutations, often suffer from sudden cardiac death (SCD) resulting from arrhythmia. In order to advance SCD prevention strategies, our understanding of how sarcomeric mutations in HCM patients contribute to enhanced arrhythmogenesis needs to be improved. Early afterdepolarizations (EADs) are an important mechanism underlying arrhythmias associated with HCM-SCD. Although the ionic mechanisms underlying EADs have been studied in general, whether myofilament protein dynamics mechanisms also underlie EADs remains unknown. Thus, our goals were to investigate if myofilament protein dynamics mechanisms underlie EADs and to uncover how those mechanisms are affected by pacing rate, sarcomere length (SL), and different levels of HCM-induced myofilament remodeling. To achieve this, a mechanistically-based bidirectionally coupled human electrophysiology-force myocyte model under the conditions of HCM was constructed. HCM ionic remodeling included a reduced repolarization reserve, while HCM myofilament modeling involved altered thin filament activation. We found that the mechanoelectric feedback (MEF) on calcium dynamics in the bidirectionally coupled model, via Troponin C buffering of cytoplasmic Ca

Indexed as

Electrophysiological PhenomenaBiomechanical PhenomenaCardiomyopathy, HypertrophicHumansMuscle ProteinsMutationMyofibrilsSarcomeresMuscle ProteinsArrhythmiaComputer modelingEarly afterdepolarizationsHypertrophic cardiomyopathyMechanoelectric feedback

Identifiers

PMID28648627
PMCPMC5716843
OpenAlexW2707100557

What OpenQuestion holds

Textmetadata
LicenceTDM
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.