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Cited by 403

The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.

Gap Junctions in Cardiovascular Disease

Jongsma, Habo J., Wilders, Ronald·2000·Circulation Research

Abstract

Abstract —Connexins, the protein molecules forming gap junction channels, are reduced in number or redistributed from intercalated disks to lateral cell borders in a variety of cardiac diseases. This “gap junction remodeling” is considered to be arrhythmogenic. Using a simple model of human ventricular myocardium, we found that quantitative remodeling data extracted from the literature gave rise to only small to moderate changes in conduction velocity and the anisotropy ratio. Especially for longitudinal conduction, cytoplasmic resistivity (and thus cellular geometry) is much more important than commonly realized. None of the remodeling data gave rise to slow conduction on the order of a few centimeters per second.

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Metadata

Authors
Jongsma, H. J., & Wilders, R.
Venue
Circulation Research
Published
2000-06-23
Volume
86
Issue
12
Pages
1193-1197
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2117689702
Cited by
403
References
42
FWCI
5.97
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Gap Junctions in Cardiovascular Disease. https://app.cochat.ai/papers/10.1161/01.res.86.12.1193
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Jongsma, H. J., & Wilders, R. (2000). Gap Junctions in Cardiovascular Disease. Circulation Research. https://doi.org/10.1161/01.res.86.12.1193

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.