ArticleProceedings of the National Academy of Sciences of the United States of America2004
Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.
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Who cites it
141 citing papers in PubMed, 295 citations in OpenAlex.
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- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- GATA factor Serpent promotes phagocytosis in non-professional phagocytes during Drosophila oogenesis.Development (Cambridge, England) · 2025Article
- Natural products targeting regulated cell deaths for adriamycin-induced cardiotoxicity.Cell death discovery · 2025Review
- The role of GATA4 in mesenchymal stem cell senescence: A new frontier in regenerative medicine.Regenerative therapy · 2025Review
- GATA4 downregulation enhances CCL20-mediated immunosuppression in hepatocellular carcinoma.Hepatology communications · 2024Article
- Doxorubicin-induced cardiotoxicity and risk factors.International journal of cardiology. Heart & vasculature · 2024Article
- Switching of hypertrophic signalling towards enhanced cardiomyocyte identity and maturity by a GATA4-targeted compound.Stem cell research & therapy · 2024Article
- KnockdownFrontiers in pharmacology · 2024Article
- Carnosic acid mitigates doxorubicin-induced cardiac toxicity: Evidence from animal and cell model investigations.Iranian journal of basic medical sciences · 2024Article
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- Bicuspid Aortic Valve-Associated Regulatory Regions RevealArteriosclerosis, thrombosis, and vascular biology · 2023Article
- Dasatinib targets c-Src kinase in cardiotoxicity.Toxicology reports · 2023Article
- Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes.BMC molecular and cell biology · 2022Article
81 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.