The DOI matches its Crossref record; 99 of the 99 references it cites were found in a registry or an index.
Remodelling of gap junctions and connexin expression in diseased myocardium
Open accessAbstract
Gap junctions form the cell-to-cell pathways for propagation of the precisely orchestrated patterns of current flow that govern the regular rhythm of the healthy heart. As in most tissues and organs, multiple connexin types are expressed in the heart: connexin43 (Cx43), Cx40 and Cx45 are found in distinctive combinations and relative quantities in different, functionally-specialized subsets of cardiac myocyte. Mutations in genes that encode connexins have only rarely been identified as being a cause of human cardiac disease, but remodelling of connexin expression and gap junction organization are well documented in acquired adult heart disease, notably ischaemic heart disease and heart failure. Remodelling may take the form of alterations in (i) the distribution of gap junctions and (ii) the amount and type of connexins expressed. Heterogeneous reduction in Cx43 expression and disordering in gap junction distribution feature in human ventricular disease and correlate with electrophysiologically identified arrhythmic changes and contractile dysfunction in animal models. Disease-related alterations in Cx45 and Cx40 expression have also been reported, and some of the functional implications of these are beginning to emerge. Apart from ventricular disease, various features of gap junction organization and connexin expression have been implicated in the initiation and persistence of the most common form of atrial arrhythmia, atrial fibrillation, though the disparate findings in this area remain to be clarified. Other major tasks ahead focus on the Purkinje/working ventricular myocyte interface and its role in normal and abnormal impulse propagation, connexin-interacting proteins and their regulatory functions, and on defining the precise functional properties conferred by the distinctive connexin co-expression patterns of different myocyte types in health and disease.
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Cites
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Gap junctions and the connexin protein family
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Cited by
Connexin 43 connexon to gap junction transition is regulated by zonula occludens-1
Rhett, J. M., Jourdan, J., & Gourdie, R. G. (2011) · Molecular Biology of the Cell · doi:10.1091/mbc.e10-06-0548 · Cited by 279
Paznekas, W. A., Karczeski, B., Vermeer, S., Lowry, R. B., Delatycki, M., Laurence, F., Koivisto, P. A., Van Maldergem, L., Boyadjiev, S. A., Bodurtha, J. N., et al. (2009) · Human Mutation · doi:10.1002/humu.20958 · Cited by 264
Translational strategies and challenges in regenerative medicine
Dimmeler, S., Ding, S., Rando, T. A., & Trounson, A. (2014) · Nature Medicine · doi:10.1038/nm.3627 · Cited by 179
Cardiac-specific deletion of LKB1 leads to hypertrophy and dysfunction
Ikeda, Y., Sato, K., Pimentel, D. R., Sam, F., Shaw, R. J., Dyck, J. R. B., & Walsh, K. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.057273 · Cited by 164
Biomechanics of Cardiac Electromechanical Coupling and Mechanoelectric Feedback
Pfeiffer, E. R., Tangney, J. R., Omens, J. H., & McCulloch, A. D. (2014) · Journal of Biomechanical Engineering · doi:10.1115/1.4026221 · Cited by 131
Metadata
- Authors
- Severs, N. J., Bruce, A. F., Dupont, E., & Rothery, S.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-08-09
- Volume
- 80
- Issue
- 1
- Pages
- 9-19
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2001535302
- Cited by
- 560
- References
- 99
- FWCI
- 11.04
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Severs, N. J., Bruce, A. F., Dupont, E., & Rothery, S. (2008). Remodelling of gap junctions and connexin expression in diseased myocardium. Cardiovascular Research. https://doi.org/10.1093/cvr/cvn133
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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