The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Differential regulation of two types of intracellular calcium release channels during end-stage heart failure.
Open accessAbstract
The molecular basis of human heart failure is unknown. Alterations in calcium homeostasis have been observed in failing human heart muscles. Intracellular calcium-release channels regulate the calcium flux required for muscle contraction. Two forms of intracellular calcium-release channels are expressed in the heart: the ryanodine receptor (RyR) and the inositol 1,4,5-trisphosphate receptor (IP3R). In the present study we showed that these two cardiac intracellular calcium release channels were regulated in opposite directions in failing human hearts. In the left ventricle, RyR mRNA levels were decreased by 31% (P < 0.025) whereas IP3R mRNA levels were increased by 123% (P < 0.005). In situ hybridization localized both RyR and IP3R mRNAs to human cardiac myocytes. The relative amounts of IP3 binding sites increased approximately 40% compared with ryanodine binding sites in the failing heart. RyR down-regulation could contribute to impaired contractility; IP3R up regulation may be a compensatory response providing an alternative pathway for mobilizing intracellular calcium release, possibly contributing to the increased diastolic tone associated with heart failure and the hypertrophic response of failing myocardium.
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Cites
Inositol trisphosphate and calcium signalling
Berridge, M. J. (1993) · Nature · doi:10.1038/361315a0 · Cited by 6,545
The natural history of congestive heart failure: the Framingham study
McKee, P. A., Castelli, W. P., McNamara, P. M., & Kannel, W. B. (1971) · New England Journal of Medicine · doi:10.1056/nejm197112232852601 · Cited by 3,448
Primary structure and expression from complementary DNA of skeletal muscle ryanodine receptor
Takeshima, H., Nishimura, S., Matsumoto, T., Ishida, H., Kangawa, K., Minamino, N., Matsuo, H., Ueda, M., Hanaoka, M., Hirose, T., et al. (1989) · Nature · doi:10.1038/339439a0 · Cited by 1,146
Goldstein, R. E., Boccuzzi, S. J., Cruess, D., & Nattel, S. (1991) · Circulation · doi:10.1161/01.cir.83.1.52 · Cited by 521
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Abdellatif, M., Sedej, S., Carmona-Gutierrez, D., Madeo, F., & Kroemer, G. (2018) · Circulation Research · doi:10.1161/circresaha.118.312208 · Cited by 239
Gong, Y., Lin, J., Ma, Z., Yu, M., Wang, M., Lai, D., & Fu, G. (2021) · Life Sciences · doi:10.1016/j.lfs.2021.119511 · Cited by 58
McCloskey, D. T., Turnbull, L., Swigart, P. M., Zambon, A. C., Turcato, S., Joho, S., Grossman, W., Conklin, B. R., Simpson, P. C., & Baker, A. J. (2005) · Physiological Genomics · doi:10.1152/physiolgenomics.00016.2005 · Cited by 33
Metadata
- Authors
- Go, L. O., Moschella, M. C., Watras, J., Handa, K. K., Fyfe, B. S., & Marks, A. R.
- Venue
- Journal of Clinical Investigation
- Published
- 1995-02-01
- Volume
- 95
- Issue
- 2
- Pages
- 888-894
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2014843536
- Cited by
- 247
- References
- 4
- FWCI
- 9.15
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Go, L. O., Moschella, M. C., Watras, J., Handa, K. K., Fyfe, B. S., & Marks, A. R. (1995). Differential regulation of two types of intracellular calcium release channels during end-stage heart failure. Journal of Clinical Investigation. https://doi.org/10.1172/jci117739
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