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Cited by 296

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity

Open access
Aries, Anne, Paradis, Pierre, Lefebvre, Chantal, Schwartz, Robert J., Nemer, Mona·2004·Proceedings of the National Academy of Sciences

Abstract

In recent years, significant progress has been made in understanding cardiomyocyte differentiation. However, little is known about the regulation of myocyte survival despite the fact that myocyte apoptosis is a leading cause of heart failure. Here we report that transcription factor GATA-4 is a survival factor for differentiated, postnatal cardiomyocytes and an upstream activator of the antiapoptotic gene Bcl-X. An early event in the cardiotoxic effect of the antitumor drug doxorubicin is GATA-4 depletion, which in turn causes cardiomyocyte apoptosis. Mouse heterozygotes for a null Gata4 allele have enhanced susceptibility to doxorubicin cardiotoxicity. Genetic or pharmacologic enhancement of GATA-4 prevents cardiomyocyte apoptosis and drug-induced cardiotoxicity. The results indicate that GATA-4 is an antiapoptotic factor required for the adaptive stress response of the adult heart. Modulation of survival/apoptosis genes by tissue-specific transcription factors may be a general paradigm that can be exploited effectively for cell-specific regulation of apoptosis in disease states.

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Metadata

Authors
Aries, A., Paradis, P., Lefebvre, C., Schwartz, R. J., & Nemer, M.
Venue
Proceedings of the National Academy of Sciences
Published
2004-04-20
Volume
101
Issue
18
Pages
6975-6980
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2124126928
Cited by
296
References
4
FWCI
9.29
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity. https://app.cochat.ai/papers/10.1073/pnas.0401833101
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Aries, A., Paradis, P., Lefebvre, C., Schwartz, R. J., & Nemer, M. (2004). Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0401833101

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