ArticleThe American journal of pathology2001
Transgenic mice with cardiac-specific expression of activating transcription factor 3, a stress-inducible gene, have conduction abnormalities and contractile dysfunction.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 102 citations in OpenAlex.
- Temporal AI model predicts drivers of cell state trajectories across human aging.bioRxiv : the preprint server for biology · 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
- Article
- Cardiac Dysfunction Promotes Cancer Progression via Multiple Secreted Factors.Cancer research · 2022Article
- Transcriptome-wide analysis reveals the molecular mechanisms of cannabinoid type II receptor agonists in cardiac injury induced by chronic psychological stress.Frontiers in genetics · 2022Article
- JDP2, a Novel Molecular Key in Heart Failure and Atrial Fibrillation?International journal of molecular sciences · 2021Review
- ATF3 expression in cardiomyocytes and myofibroblasts following transverse aortic constriction displays distinct phenotypes.International journal of cardiology. Heart & vasculature · 2021Article
- Article
- Activating transcription factor 3 coordinates differentiation of cardiac and hematopoietic progenitors by regulating glucose metabolism.Science advances · 2020Article
- HDAC (Histone Deacetylase) Inhibitor Valproic Acid Attenuates Atrial Remodeling and Delays the Onset of Atrial Fibrillation in Mice.Circulation. Arrhythmia and electrophysiology · 2019Article
- JDP2 and ATF3 deficiencies dampen maladaptive cardiac remodeling and preserve cardiac function.PloS one · 2019Article
- ATF3 Regulates the Expression of AChE During Stress.Frontiers in molecular neuroscience · 2018Article
- Cardiac fibrosis: new insights into the pathogenesis.International journal of biological sciences · 2018 · on this mapReview
- Homozygous CREM-IbΔC-X Overexpressing Mice Are a Reliable and Effective Disease Model for Atrial Fibrillation.Frontiers in pharmacology · 2018Article
- Putting the Brakes on Hypertensive Remodeling: An ATF3 Mechanism of Myofibroblast Restraint.Circulation · 2017Article
- Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.Molecular and cellular biochemistry · 2017Review
- Induction of activating transcription factor 3 limits survival following infarct-induced heart failure in mice.American journal of physiology. Heart and circulatory physiology · 2015Article
- Genome-wide mRNA expression profiling in vastus lateralis of COPD patients with low and normal fat free mass index and healthy controls.Respiratory research · 2015Article
- Modelling negative feedback networks for activating transcription factor 3 predicts a dominant role for miRNAs in immediate early gene regulation.PLoS computational biology · 2014Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Activating transcription factor 3 (ATF3) is a member of the CREB/ATF family of transcription factors. Previously, we demonstrated that the expression of the ATF3 gene is induced by many stress signals. In this report, we demonstrate that expression of ATF3 is induced by cardiac ischemia coupled with reperfusion (ischemia-reperfusion) in both cultured cells and an animal model. Transgenic mice expressing ATF3 under the control of the alpha-myosin heavy chain promoter have atrial enlargement, and atrial and ventricular hypertrophy. Microscopic examination showed myocyte degeneration and fibrosis. Functionally, the transgenic heart has reduced contractility and aberrant conduction. Interestingly, expression of sorcin, a gene whose product inhibits the release of calcium from sarcoplasmic reticulum, is increased in these transgenic hearts. Taken together, our results indicate that expression of ATF3, a stress-inducible gene, in the heart leads to altered gene expression and impaired cardiac function.
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