The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Signaling effectors underlying pathologic growth and remodeling of the heart
Open accessAbstract
Cardiovascular disease is the number one cause of mortality in the Western world.The heart responds to many cardiopathological conditions with hypertrophic growth by enlarging individual myocytes to augment cardiac pump function and decrease ventricular wall tension.Initially, such cardiac hypertrophic growth is often compensatory, but as time progresses these changes become maladaptive.Cardiac hypertrophy is the strongest predictor for the development of heart failure, arrhythmia, and sudden death.Here we discuss therapeutic avenues emerging from molecular and genetic studies of cardiovascular disease in animal models.The majority of these are based on intracellular signaling pathways considered central to pathologic cardiac remodeling and hypertrophy, which then leads to heart failure.We focus our discussion on selected therapeutic targets that have more recently emerged and have a tangible translational potential given the available pharmacologic agents that could be readily evaluated in human clinical trials.β-Adrenergic receptor signaling and associated kinases in cardiac hypertrophy and remodeling Inhibition of β-adrenergic receptor signaling is perhaps the most effective and frequently employed therapy in addressing negative Conflict of interest:The authors have declared that no conflict of interest exists.
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Cites
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“…signaling pathways that have emerged more recently from mechanistic and genetic studies in animal models of cardiac remodeling that offer new treatment opportunities. cardiac remodeling associated with hypertension, postmyocardial infarction remodeling, or early stages of heart failure (27–30).”
Differential regulation and properties of MAPKs
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“Additional side branches in this cascade include ERK5 and its upstream activator MEK5, as well as ERK3/4, although the upstream regulatory kinases for these effectors are not well characterized (94, 95).”
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Cited by
Molecular basis of physiological heart growth: fundamental concepts and new players
Maillet, M., van Berlo, J. H., & Molkentin, J. D. (2013) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3495 · Cited by 536
Self-citationBET Bromodomains Mediate Transcriptional Pause Release in Heart Failure
Anand, P., Brown, J. D., Lin, C. Y., Qi, J., Zhang, R., Artero, P. C., Alaiti, M. A., Bullard, J., Alazem, K., Margulies, K. B., et al. (2013) · Cell · doi:10.1016/j.cell.2013.07.013 · Cited by 406
Cardiac Resident Macrophages Prevent Fibrosis and Stimulate Angiogenesis
Revelo, X. S., Parthiban, P., Chen, C., Barrow, F., Fredrickson, G., Wang, H., Yücel, D., Herman, A., & van Berlo, J. H. (2021) · Circulation Research · doi:10.1161/circresaha.121.319737 · Cited by 298
Self-citationDuan, Q., McMahon, S., Anand, P., Shah, H., Thomas, S., Salunga, H. T., Huang, Y., Zhang, R., Sahadevan, A., Lemieux, M. E., et al. (2017) · Science Translational Medicine · doi:10.1126/scitranslmed.aah5084 · Cited by 262
Cardiac Nonmyocytes in the Hub of Cardiac Hypertrophy
Kamo, T., Akazawa, H., & Komuro, I. (2015) · Circulation Research · doi:10.1161/circresaha.117.305349 · Cited by 171
Metadata
- Authors
- van Berlo, J. H., Maillet, M., & Molkentin, J. D.
- Venue
- Journal of Clinical Investigation
- Published
- 2013-01-02
- Volume
- 123
- Issue
- 1
- Pages
- 37-45
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2167407855
- Cited by
- 445
- References
- 8
- FWCI
- 33.47
- 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).
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