The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Mechanisms of Altered Ca 2+ Handling in Heart Failure
Open accessAbstract
Ca 2+ plays a crucial role in connecting membrane excitability with contraction in myocardium. The hallmark features of heart failure are mechanical dysfunction and arrhythmias; defective intracellular Ca 2+ homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca 2+ homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca 2+ homeostatic and structural proteins, ion channels, and enzymes. This review focuses on the molecular mechanisms of defective Ca 2+ cycling in heart failure and considers how fundamental understanding of these pathways may translate into novel and innovative therapies.
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Cited by
Bhattacharyya, M., Stratton, M. M., Going, C. C., McSpadden, E. D., Huang, Y., Susa, A. C., Elleman, A., Cao, Y. M., Pappireddi, N., Burkhardt, P., et al. (2016) · eLife · doi:10.7554/elife.13405 · Cited by 112
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Joseph, L. C., Subramanyam, P., Radlicz, C., Trent, C. M., Iyer, V., Colecraft, H. M., & Morrow, J. P. (2016) · Heart Rhythm · doi:10.1016/j.hrthm.2016.05.002 · Cited by 60
Is hydrogen ion (H+) the real second messenger in calcium signalling?
Molinari, G. (2015) · Cellular Signalling · doi:10.1016/j.cellsig.2015.03.023 · Cited by 13
Metadata
- Authors
- Luo, M., & Anderson, M. E.
- Venue
- Circulation Research
- Published
- 2013-08-30
- Volume
- 113
- Issue
- 6
- Pages
- 690-708
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2118103758
- Cited by
- 357
- References
- 14
- FWCI
- 16.74
- Type
- journal article
- Language
- en
- Open access
- bronze
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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.
