The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte Viability
Open accessAbstract
The transcription factor GATA4 is a critical regulator of cardiac gene expression where it controls embryonic development, cardiomyocyte differentiation, and stress responsiveness of the adult heart. Traditional deletion of Gata4 caused embryonic lethality associated with endoderm defects and cardiac malformations, precluding an analysis of the role of GATA4 in the adult myocardium. To address the function of GATA4 in the adult heart, Gata4-loxP –targeted mice ( Gata4fl/fl ) were crossed with mice containing a β-myosin heavy chain (β-MHC) or α-MHC promoter-driven Cre transgene, which produced viable mice that survived into adulthood despite a 95% and 70% loss of GATA4 protein, respectively. However, cardiac-specific deletion of Gata4 resulted in a progressive and dosage-dependent deterioration in cardiac function and dilation in adulthood. Moreover, pressure overload stimulation induced rapid decompensation and heart failure in cardiac-specific Gata4 -deleted mice. More provocatively, Gata4 -deleted mice were compromised in their ability to hypertrophy following pressure overload or exercise stimulation. Mechanistically, cardiac-specific deletion of Gata4 increased cardiomyocyte TUNEL at baseline in embryos and adults as they aged, as well as dramatically increased TUNEL following pressure overload stimulation. Examination of gene expression profiles in the heart revealed a number of profound alterations in known GATA4-regulated structural genes as well as genes with apoptotic implications. Thus, GATA4 is a necessary regulator of cardiac gene expression, hypertrophy, stress-compensation, and myocyte viability.
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Citations
Cites
GATA4 mutations cause human congenital heart defects and reveal an interaction with TBX5
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Self-citationGATA4 transcription factor is required for ventral morphogenesis and heart tube formation.
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Self-citationCalcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy
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Self-citationTranscriptional regulation and function during the human cell cycle
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Self-citationGATA4 is essential for formation of the proepicardium and regulates cardiogenesis
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Nicolás-Ávila, J. A., Lechuga-Vieco, A. V., Esteban-Martínez, L., Sánchez-Díaz, M., Díaz-García, E., Santiago, D. J., Rubio-Ponce, A., Li, J. L., Balachander, A., Quintana, J. A., et al. (2020) · Cell · doi:10.1016/j.cell.2020.08.031 · Cited by 762
Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart
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The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability
Luongo, T. S., Lambert, J. P., Gross, P., Nwokedi, M., Lombardi, A. A., Shanmughapriya, S., Carpenter, A. C., Kolmetzky, D., Gao, E., van Berlo, J. H., et al. (2017) · Nature · doi:10.1038/nature22082 · Cited by 396
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Metadata
- Authors
- Oka, T., Maillet, M., Watt, A. J., Schwartz, R. J., Aronow, B. J., Duncan, S. A., & Molkentin, J. D.
- Venue
- Circulation Research
- Published
- 2006-03-31
- Volume
- 98
- Issue
- 6
- Pages
- 837-845
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2154201149
- Cited by
- 423
- References
- 30
- FWCI
- 7.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Oka, T., Maillet, M., Watt, A. J., Schwartz, R. J., Aronow, B. J., Duncan, S. A., & Molkentin, J. D. (2006). Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte Viability. Circulation Research. https://doi.org/10.1161/01.res.0000215985.18538.c4
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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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