ArticleHypertension (Dallas, Tex. : 1979)2010
Pulmonary hypertension-induced GATA4 activation in the right ventricle.
Article in Hypertension (Dallas, Tex. : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Targeting senescence and GATA4 in age-related cardiovascular disease: a comprehensive approach.Biogerontology · 2025Review
- The Role of Early Child Nutrition in Pulmonary Hypertension-A Narrative Review.Children (Basel, Switzerland) · 2024Review
- Molecular remodeling in comorbidities associated with heart failure: a current update.Molecular biology reports · 2024Review
- Pulmonary Hypertension and Right Ventricle: A Pathophysiological Insight.Clinical Medicine Insights. Cardiology · 2024Review
- Potential Roles of Metals in the Pathogenesis of Pulmonary and Systemic Hypertension.International journal of biological sciences · 2023Review
- The role of post-translational modifications in driving abnormal cardiovascular complications at high altitude.Frontiers in cardiovascular medicine · 2022Review
- Review
- Oxidative Stress and Its Implications in the Right Ventricular Remodeling Secondary to Pulmonary Hypertension.Frontiers in physiology · 2019Review
- Effects of Bcl-2/Bcl-xAntioxidants (Basel, Switzerland) · 2018Article
- Redox Biology of Right-Sided Heart Failure.Antioxidants (Basel, Switzerland) · 2018Review
- Steroid receptor coactivator-2 (SRC-2) coordinates cardiomyocyte paracrine signaling to promote pressure overload-induced angiogenesis.The Journal of biological chemistry · 2017Article
- Docetaxel Reverses Pulmonary Vascular Remodeling by Decreasing Autophagy and Resolves Right Ventricular Fibrosis.The Journal of pharmacology and experimental therapeutics · 2017Article
- Natural reversal of pulmonary vascular remodeling and right ventricular remodeling in SU5416/hypoxia-treated Sprague-Dawley rats.PloS one · 2017Article
- Article
- Hemodynamic response to treatment of iron deficiency anemia in pulmonary arterial hypertension: longitudinal insights from an implantable hemodynamic monitor.Pulmonary circulation · 2016Article
- Modulators of right ventricular apoptosis and contractility in a rat model of pulmonary hypertension.Cardiovascular research · 2016Article
- Apoptosis-based therapy to treat pulmonary arterial hypertension.Journal of rare diseases research & treatment · 2016Article
- Differential stress response mechanisms in right and left ventricles.Journal of rare diseases research & treatment · 2016Article
- Transcriptional regulation of α1H T-type calcium channel under hypoxia.American journal of physiology. Cell physiology · 2014Article
- Pressure-overload-induced right heart failure.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The major cause of death among pulmonary hypertension patients is right heart failure, but the biology of right heart is not well understood. Previous studies showed that mechanisms of the activation of GATA4, a major regulator of cardiac hypertrophy, in response to pressure overload are different between left and right ventricles. In the left ventricle, aortic constriction triggers GATA4 activation via posttranslational modifications without influencing GATA4 expression, while pulmonary artery banding enhances GATA4 expression in the right ventricle. We found that GATA4 expression can also be increased in the right ventricle of rats treated with chronic hypoxia to induce pulmonary hypertension and investigated the mechanism of increased GATA4 expression. Examination of Gata4 promoter revealed that CCAAT box plays an important role in gene activation, and hypoxic pulmonary hypertension promoted the binding of CCAAT-binding factor/nuclear factor-Y (CBF/NF-Y) to CCAAT box in the right ventricle. We found that CBF/NF-Y forms a complex with annexin A1, which inhibits DNA binding activity. In response to hypoxic pulmonary hypertension, annexin A1 gets degraded, resulting in CBF/NF-Y-dependent activation of Gata4 gene transcription. The right ventricle contains a higher level of CBF/NF-Y compared to the left ventricle, and this may allow for efficient activation in response to annexin A1 degradation. Signaling via iron-catalyzed protein oxidation mediates hypoxic pulmonary hypertension-induced annexin A1 degradation, Gata4 gene transcription, and right ventricular hypertrophy. These results establish a right heart-specific signaling mechanism in response to pressure overload, which involves metal-catalyzed carbonylation and degradation of annexin A1 that liberates CBF/NF-Y to activate Gata4 gene transcription.
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Registered trials
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