Evidence map›Paper›PMID 38797242›Full record

ReviewJournal of molecular and cellular cardiology2024

Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.

Roman Y Medvedev, Saheed O Afolabi, Daniel G P Turner, Alexey V Glukhov

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Downregulation of L-type CaHeart rhythm · 2026
    Article
  4. Osteopontin in Atrial Fibrillation and Atrial Remodeling.Journal of the American Heart Association · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. 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

4 authors.

Roman Y MedvedevDepartment of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA.
Saheed O AfolabiDepartment of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA; Department of Pharmacology and Therapeutics, University of Ilorin, Ilorin, Nigeria.
Daniel G P TurnerDepartment of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA.
Alexey V GlukhovDepartment of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA. Electronic address: aglukhov@medicine.wisc.edu.

Funding

Functional Microdomains in the Heart's Pacemaker: A New Dimension of Cardiac RemodelingR01HL141214 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Alexey V Glukhov · 2018 to 2026
$3.8M
Multiomics and Functional Characterization Establish Druggable Targets for PVC-Driven Idiopathic VFR01HL170521 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Lee Lochbaum Eckhardt, Eleonora Grandi · 2023 to 2026
$3.1M
KCNJ2-Induced Arrhythmia Mechanisms in CPVT and Heart Failure.R01HL139738 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI ECKHARDT, LEE LOCHBAUM · 2018 to 2021
$1.5M
Engineered Anisotropic and Vascularized Human Cardiac PatchR01HL146652 · NHLBI · TEXAS ENGINEERING EXPERIMENT STATION · PI ZHAO, FENG · 2020 to 2023
$1.4M
NHLBI NIH HHS R01 HL139738NHLBI NIH HHS R01 HL141214NHLBI NIH HHS R01 HL146652NHLBI NIH HHS R01 HL170521
6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common cardiac rhythm disorder, often occurring in the setting of atrial distension and elevated myocardialstretch. While various mechano-electrochemical signal transduction pathways have been linked to AF development and progression, the underlying molecular mechanisms remain poorly understood, hampering AF therapies. In this review, we describe different aspects of stretch-induced electro-anatomical remodeling as seen in animal models and in patients with AF. Specifically, we focus on cellular and molecular mechanisms that are responsible for mechano-electrochemical signal transduction and the development of ectopic beats triggering AF from pulmonary veins, the most common source of paroxysmal AF. Furthermore, we describe structural changes caused by stretch occurring before and shortly after the onset of AF as well as during AF progression, contributing to longstanding forms of AF. We also propose mechanical stretch as a new dimension to the concept "AF begets AF", in addition to underlying diseases. Finally, we discuss the mechanisms of these electro-anatomical alterations in a search for potential therapeutic strategies and the development of novel antiarrhythmic drugs targeted at the components of mechano-electrochemical signal transduction not only in cardiac myocytes, but also in cardiac non-myocyte cells.

Indexed as

Atrial FibrillationAnimalsAtrial RemodelingElectrophysiological PhenomenaHeart AtriaHumansMyocytes, CardiacPulmonary VeinsSignal TransductionAtriaAtrial fibrillationCalciumCardiomyocyteElectro-anatomical remodelingFibrosisHypertensionStretch

Identifiers

PMID38797242
PMCPMC11260238

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Registered trials

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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.