Evidence map›Paper›PMID 41885641›Full record

ArticleThe Journal of physiology2026

Ephaptic coupling and the source-sink effect of cardiac conduction.

Jingwu Pan, Peter Hanna, Alan Garfinkel, Kalyanam Shivkumar, Zhilin Qu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Cardiac Impulse Propagation: An Integrated View.JACC. Basic to translational science · 2026
    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

5 authors.

Jingwu PanDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Peter HannaDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Alan GarfinkelDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Kalyanam ShivkumarDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Zhilin QuDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.

Funding

Neural Control of Myocardial Excitability at the Nerve Myocyte InterfaceP01HL164311 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KALYANAM SHIVKUMAR · 2023 to 2026
$11.3M
A population-based computational approach for arrhythmia prediction and therapyR01HL175074 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZHILIN QU · 2024 to 2026
$1.2M
NHLBI NIH HHS P01 HL164311NHLBI NIH HHS R01 HL175074
6 · The paper itself

Abstract

As a result of the electrotonic effect, under gap junction coupling, a critical number of excited cells is needed to elicit electrical conduction in cardiac tissue, a phenomenon called the source-sink effect. However, it is unclear how ephaptic coupling affects the source-sink effect. To address this issue, we carry out computer simulations to investigate the effects of ephaptic coupling and its interaction with gap junction coupling on conduction triggered by the following types of depolarization: (i) an external stimulation; (ii) a delayed afterdepolarization; and (iii) automaticity. Simulations were carried out using a one-dimensional cable with the presence of a cleft between two adjacent myocytes and junctional ion channel distributions. We show that: (i) under pure ephaptic coupling, only one stimulated cell is needed to elicit conduction, implying that there is no source-sink effect; (i) the minimum number of stimulated (or delayed afterdepolarization or oscillatory) cells needed to elicit a conduction increases as gap junction conductance increases, as predicted by the gap junction coupling theory; and (iii) the dependence of the source-sink effect on the cleft width exhibits complex behaviours, which are mainly caused by self-attenuation of the junctional sodium current as a result of the ephaptic effect and self-enhancement of the junctional inward rectifier potassium current as a result of an increase of potassium concentration in the cleft. In conclusion, ephaptic coupling and cleft width play non-trivial roles in the source-sink effect of cardiac conduction and thus may be non-trivial for arrhythmogenesis under disease conditions in which gap junctions and cleft structure are altered. KEY POINTS: Gap junction coupling is recognized as the primary mechanism of cardiac conduction, but ephaptic coupling may also play a non-trivial role. Source-sink effects are a key feature of cardiac conduction, and it is unclear how they are affected by ephaptic coupling. Computer simulations are used to investigate how source-sink effects are altered by ephaptic coupling and its interaction with gap junction coupling. Under pure ephaptic coupling, only one stimulated cell is needed to elicit conduction, implying that there is no source-sink effect. The minimum number of depolarized cells needed to elicit a conduction exhibits complex behaviours and depends on the manner of depolarization. These effects are mainly caused by self-attenuation of the junctional sodium current as a result of the ephaptic effect and self-enhancement of the inward rectifier potassium current as a result of increase of potassium concentration in the cleft.

Indexed as

Gap JunctionsHeart Conduction SystemModels, CardiovascularMyocytes, CardiacAction PotentialsAnimalsComputer SimulationHumanscardiac conductionephaptic couplinggap junction couplingintercalated discsource–sink effect

Identifiers

PMID41885641
PMCPMC13189686

What Socratic holds

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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 Socratic graph.