The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
CaMKII in myocardial hypertrophy and heart failure
Open accessAbstract
Many signals have risen and fallen in the tide of investigation into mechanisms of myocardial hypertrophy and heart failure (HF). In our opinion, the multifunctional Ca and calmodulin-dependent protein kinase II (CaMKII) has emerged as a molecule to watch, in part because a solid body of accumulated data essentially satisfy Koch's postulates, showing that the CaMKII pathway is a core mechanism for promoting myocardial hypertrophy and heart failure. Multiple groups have now confirmed the following: (1) that CaMKII activity is increased in hypertrophied and failing myocardium from animal models and patients; (2) CaMKII overexpression causes myocardial hypertrophy and HF and (3) CaMKII inhibition (by drugs, inhibitory peptides and gene deletion) improves myocardial hypertrophy and HF. Patients with myocardial disease die in equal proportion from HF and arrhythmias, and a major therapeutic obstacle is that drugs designed to enhance myocardial contraction promote arrhythmias. In contrast, inhibiting the CaMKII pathway appears to reduce arrhythmias and improve myocardial responses to pathological stimuli. This brief paper will introduce the molecular physiology of CaMKII and discuss the impact of CaMKII on ion channels, Ca handling proteins and transcription in myocardium. This article is part of a Special Issue entitled “Key Signaling Molecules Special Issue”.
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1 retracted
RETRACTED: L-Type Ca2+ Channel Facilitation Mediated by Phosphorylation of the β Subunit by CaMKII
Grueter, C. E., Abiria, S. A., Dzhura, I., Wu, Y., Ham, A.-J. L., Mohler, P. J., Anderson, M. E., & Colbran, R. J. (2006) · Molecular Cell · doi:10.1016/j.molcel.2006.07.006 · Cited by 184
Self-citationRetractedSensitivity of CaM Kinase II to the Frequency of Ca 2+ Oscillations
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A Dynamic Pathway for Calcium-Independent Activation of CaMKII by Methionine Oxidation
Erickson, J. R., Joiner, M.-L. A., Guan, X., Kutschke, W., Yang, J., Oddis, C. V., Bartlett, R. K., Lowe, J. S., O'Donnell, S. E., Aykin-Burns, N., et al. (2008) · Cell · doi:10.1016/j.cell.2008.02.048 · Cited by 1,122
Self-citationClass II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy
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Self-citationMethionine sulfoxide reductase (MsrA) is a regulator of antioxidant defense and lifespan in mammals
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Calmodulin Trapping by Calcium-Calmodulin-Dependent Protein Kinase
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Calmodulin kinase II inhibition protects against structural heart disease
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Cited by
Tham, Y. K., Bernardo, B. C., Ooi, J. Y. Y., Weeks, K. L., & McMullen, J. R. (2015) · Archives of Toxicology · doi:10.1007/s00204-015-1477-x · Cited by 708
Signaling effectors underlying pathologic growth and remodeling of the heart
van Berlo, J. H., Maillet, M., & Molkentin, J. D. (2013) · Journal of Clinical Investigation · doi:10.1172/jci62839 · Cited by 445
Cell-cell communication: New insights and clinical implications
Su, J., Song, Y., Zhu, Z., Huang, X., Fan, J., Qiao, J., & Mao, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01888-z · Cited by 433
Cellular and molecular pathobiology of heart failure with preserved ejection fraction
Mishra, S., & Kass, D. A. (2021) · Nature Reviews Cardiology · doi:10.1038/s41569-020-00480-6 · Cited by 417
Mechanisms of Altered Ca 2+ Handling in Heart Failure
Luo, M., & Anderson, M. E. (2013) · Circulation Research · doi:10.1161/circresaha.113.301651 · Cited by 357
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Metadata
- Authors
- Anderson, M. E., Brown, J. H., & Bers, D. M.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 51
- Issue
- 4
- Pages
- 468-473
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W1969154199
- Cited by
- 465
- References
- 72
- FWCI
- 23.99
- Type
- journal article
- Language
- en
- Open access
- green
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