The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Cellular mechanisms of cardiomyopathy
Open accessAbstract
The heart exhibits remarkable adaptive responses to a wide array of genetic and extrinsic factors to maintain contractile function. When compensatory responses are not sustainable, cardiac dysfunction occurs, leading to cardiomyopathy. The many forms of cardiomyopathy exhibit a set of overlapping phenotypes reflecting the limited range of compensatory responses that the heart can use. These include cardiac hypertrophy, induction of genes normally expressed during development, fibrotic deposits that replace necrotic and apoptotic cardiomyocytes, and metabolic disturbances. The compensatory responses are mediated by signaling pathways that initially serve to maintain normal contractility; however, persistent activation of these pathways leads to cardiac dysfunction. Current research focuses on ways to target these specific pathways therapeutically.
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Cites
Apoptosis in the Failing Human Heart
Olivetti, G., Abbi, R., Quaini, F., Kajstura, J., Cheng, W., Nitahara, J. A., Quaini, E., Di Loreto, C., Beltrami, C. A., Krajewski, S., et al. (1997) · New England Journal of Medicine · doi:10.1056/nejm199704173361603 · Cited by 1,673
Is the Failing Heart Energy Starved?: On Using Chemical Energy to Support Cardiac Function
Ingwall, J. S., & Weiss, R. G. (2004) · Circulation Research · doi:10.1161/01.res.0000137170.41939.d9 · Cited by 604
Regulation of energy substrate metabolism in the diabetic heart
Stanley, W. (1997) · Cardiovascular Research · doi:10.1016/s0008-6363(97)00047-3 · Cited by 480
Altered creatine kinase adenosine triphosphate kinetics in failing hypertrophied human myocardium
Smith, C. S., Bottomley, P. A., Schulman, S. P., Gerstenblith, G., & Weiss, R. G. (2006) · Circulation · doi:10.1161/circulationaha.106.613646 · Cited by 204
Apoptotic myocardial cell death in the setting of arrhytmogenic right ventricular cardiomyopathy
YAMAJI, K., FUJIMOTO, S., IKEDA, Y., MASUDA, K., NAKAMURA, S., SAITO, Y., & YUTANI, C. (2005) · Acta Cardiologica · doi:10.2143/ac.60.5.2004965 · Cited by 24
Cited by
Gorski, P. A., Ceholski, D. K., & Hajjar, R. J. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.01.005 · Cited by 213
Titration of mitochondrial fusion rescues Mff -deficient cardiomyopathy
Chen, H., Ren, S., Clish, C., Jain, M., Mootha, V., McCaffery, J. M., & Chan, D. C. (2015) · Journal of Cell Biology · doi:10.1083/jcb.201507035 · Cited by 168
To divide or not to divide: revisiting liver regeneration
Miyaoka, Y., & Miyajima, A. (2013) · Cell Division · doi:10.1186/1747-1028-8-8 · Cited by 156
Fibrous scaffolds for building hearts and heart parts
Capulli, A. K., MacQueen, L. A., Sheehy, S. P., & Parker, K. K. (2016) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2015.11.020 · Cited by 130
Current management of hypertrophic cardiomyopathy
Sikand, N., Stendahl, J., Sen, S., Lampert, R., & Day, S. (2025) · BMJ · doi:10.1136/bmj-2023-077274 · Cited by 26
Metadata
- Authors
- Harvey, P. A., & Leinwand, L. A.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2011-08-08
- Volume
- 194
- Issue
- 3
- Pages
- 355-365
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2121936157
- Cited by
- 360
- References
- 5
- FWCI
- 8.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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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).
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