ArticlePloS one2013
Adult cardiac expression of the activating transcription factor 3, ATF3, promotes ventricular hypertrophy.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- Metrics of left ventricular active relaxation reflect proteomic myocardial remodelling and reverse remodelling.ESC heart failure · 2026Article
- The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- ATF3 overexpression is associated with cardiac hypertrophy and electrical dysfunction accompanied by enhanced cardiac cell proliferation in zebrafish.Scientific reports · 2025Article
- Cancer-driven cytokine immunomodulation ameliorates cardiac function and suppresses fibrosis.Journal of molecular and cellular cardiology plus · 2025Article
- Investigating Left Atrial Diameter and Heart Failure Onset in Middle-Aged and Elderly: A Retrospective-Prospective Study.Clinical cardiology · 2025Article
- Contractile and Genetic Characterization of Cardiac Constructs Engineered from Human Induced Pluripotent Stem Cells: Modeling of Tuberous Sclerosis Complex and the Effects of Rapamycin.Bioengineering (Basel, Switzerland) · 2024Article
- Common biological processes and mutual crosstalk mechanisms between cardiovascular disease and cancer.Frontiers in oncology · 2024Review
- Article
- CircRNA Interference Pathway: A New Target for Intervention in Different Stages of Heart Failure.Current topics in medicinal chemistry · 2024Review
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Article
- ATF3 regulates SPHK1 in cardiomyocyte injury via endoplasmic reticulum stress.Immunity, inflammation and disease · 2023Article
- NFIXing Cancer: The Role of NFIX in Oxidative Stress Response and Cell Fate.International journal of molecular sciences · 2023Review
- ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury.International journal of molecular sciences · 2023Article
- Cardiac Dysfunction Promotes Cancer Progression via Multiple Secreted Factors.Cancer research · 2022Article
- Circ_nuclear factor I X (circNfix) attenuates pressure overload-induced cardiac hypertrophy via regulating miR-145-5p/ATF3 axis.Bioengineered · 2021Article
- Calcium Regulation on the Atrial Regional Difference of Collagen Production Activity in Atrial Fibrogenesis.Biomedicines · 2021Article
- JDP2, a Novel Molecular Key in Heart Failure and Atrial Fibrillation?International journal of molecular sciences · 2021Review
- Prediction of single-cell mechanisms for disease progression in hypertrophic remodelling by a trans-omics approach.Scientific reports · 2021Article
- ATF3 expression in cardiomyocytes and myofibroblasts following transverse aortic constriction displays distinct phenotypes.International journal of cardiology. Heart & vasculature · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is an adaptive response to various mechanophysical and pathophysiological stresses. However, when chronic stress is sustained, the beneficial response turns into a maladaptive process that eventually leads to heart failure. Although major advances in the treatment of patients have reduced mortality, there is a dire need for novel treatments for cardiac hypertrophy. Accordingly, considerable efforts are being directed towards developing mice models and understanding the processes that lead to cardiac hypertrophy. A case in point is ATF3, an immediate early transcription factor whose expression is induced in various cardiac stress models but has been reported to have conflicting functional significance in hypertrophy. To address this issue, we generated a transgenic mouse line with tetracycline-regulated ATF3 cardiac expression. These mice allowed us to study the consequence of ATF3 expression in the embryo or during the adult period, thus distinguishing the effect of ATF3 on development versus pathogenesis of cardiac dysfunction. Importantly, ATF3 expression in adult mice resulted in rapid ventricles hypertrophy, heart dysfunction, and fibrosis. When combined with a phenylephrine-infusion pressure overload model, the ATF3 expressing mice displayed a severe outcome and heart dysfunction. In a complementary approach, ATF3 KO mice displayed a lower level of heart hypertrophy in the same pressure overload model. In summary, ectopic expression of ATF3 is sufficient to promote cardiac hypertrophy and exacerbates the deleterious effect of chronic pressure overload; conversely, ATF3 deletion protects the heart. Therefore, ATF3 may serve as an important drug target to reduce the detrimental consequences of heart hypertrophy.
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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.