ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Induction of activating transcription factor 3 limits survival following infarct-induced heart failure in mice.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Fibroblast Has2 limits acute heart failure following myocardial infarction in male mice.Physiological reports · 2025Article
- Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by spatial and single-cell transcriptomics.Science advances · 2025Article
- Dietary Branched-Chain Amino Acids Modify Postinfarct Cardiac Remodeling and Function in the Murine Heart.Journal of the American Heart Association · 2025Article
- Dietary Branched Chain Amino Acids Modify Post-Infarct Cardiac Remodeling and Function in the Murine Heart.bioRxiv : the preprint server for biology · 2024Article
- ATF3 coordinates the survival and proliferation of cardiac macrophages and protects against ischemia-reperfusion injury.Nature cardiovascular research · 2024Article
- 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
- The miR526b-5p-Related Single Nucleotide Polymorphisms, rs72618599, Located in 3'-UTR of TCF3 Gene, is Associated with the Risk of Breast and Gastric CancersIranian biomedical journal · 2022Article
- ATF3 induces RAB7 to govern autodegradation in paligenosis, a conserved cell plasticity program.EMBO reports · 2021Article
- Overexpression of Activating Transcription Factor 3 Alleviates Cardiac Microvascular Ischemia/Reperfusion Injury in Rats.Frontiers in pharmacology · 2021Article
- Panax Notoginseng Saponins Inhibits Ventricular Remodeling after Myocardial Infarction in Rats Through Regulating ATF3/MAP2K3/p38 MAPK and NF κ B Pathway.Chinese journal of integrative medicine · 2020Article
- Bridging the Gap Between Diabetes and Stroke in Search of High Clinical Relevance Therapeutic Targets.Neuromolecular medicine · 2019Review
- Silk fibroin/poly(L-lactic acid-co-ε-caprolactone) electrospun nanofibrous scaffolds exert a protective effect following myocardial infarction.Experimental and therapeutic medicine · 2019Article
- Cardiac Fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction.Chinese medical journal · 2018Article
- RNAi-mediatedBioscience reports · 2017Article
- Article
- Systematic Characterization of Long Noncoding RNAs Reveals the Contrasting Coordination of Cis- and Trans-Molecular Regulation in Human Fetal and Adult Hearts.Circulation. Cardiovascular genetics · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Numerous fibrotic and inflammatory changes occur in the failing heart. Recent evidence indicates that certain transcription factors, such as activating transcription factor 3 (ATF3), are activated during heart failure. Because ATF3 may be upregulated in the failing heart and affect inflammation, we focused on the potential role of ATF3 on postinfarct heart failure. We subjected anesthetized, wild-type mice to nonreperfused myocardial infarction and observed a significant induction in ATF3 expression and nuclear translocation. To test whether the induction of ATF3 affected the severity of heart failure, we subjected wild-type and ATF3-null mice to nonreperfused infarct-induced heart failure. There were no differences in cardiac function between the two genotypes, except at the 2-wk time point; however, ATF3-null mice survived the heart failure protocol at a significantly higher rate than the wild-type mice. Similar to the slight favorable improvements in chamber dimensions at 2 wk, we also observed greater cardiomyocyte hypertrophy and more fibrosis in the noninfarcted regions of the ATF3-null hearts compared with the wild-type. Nevertheless, there were no significant group differences at 4 wk. Furthermore, we found no significant differences in markers of inflammation between the wild-type and ATF3-null hearts. Our data suggest that ATF3 suppresses fibrosis early but not late during infarct-induced heart failure. Although ATF3 deficiency was associated with more fibrosis, this did not occur at the expense of survival, which was higher in the ATF3-null mice. Overall, ATF3 may serve a largely maladaptive role during heart failure.
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