ArticlePloS one2019
JDP2 and ATF3 deficiencies dampen maladaptive cardiac remodeling and preserve cardiac function.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Reimagining periodontal regeneration: smart biomaterials for a complex tissue landscape.Regenerative biomaterials · 2026Review
- The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Article
- Article
- ATF3 regulates SPHK1 in cardiomyocyte injury via endoplasmic reticulum stress.Immunity, inflammation and disease · 2023Article
- Tumor Growth Ameliorates Cardiac Dysfunction.Cells · 2023Article
- Single-cell analysis reveals an Angpt4-initiated EPDC-EC-CM cellular coordination cascade during heart regeneration.Protein & cell · 2023Article
- Cardiac Dysfunction Promotes Cancer Progression via Multiple Secreted Factors.Cancer research · 2022Article
- Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse.Frontiers in genetics · 2022Article
- Novel and Annotated Long Noncoding RNAs Associated with Ischemia in the Human Heart.International journal of molecular sciences · 2021Article
- 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
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Jun dimerization protein (JDP2) and Activating Transcription Factor 3 (ATF3) are closely related basic leucine zipper proteins. Transgenic mice with cardiac expression of either JDP2 or ATF3 showed maladaptive remodeling and cardiac dysfunction. Surprisingly, JDP2 knockout (KO) did not protect the heart following transverse aortic constriction (TAC). Instead, the JDP2 KO mice performed worse than their wild type (WT) counterparts. To test whether the maladaptive cardiac remodeling observed in the JDP2 KO mice is due to ATF3, ATF3 was removed in the context of JDP2 deficiency, referred as double KO mice (dKO). Mice were challenged by TAC, and followed by detailed physiological, pathological and molecular analyses. dKO mice displayed no apparent differences from WT mice under unstressed condition, except a moderate better performance in dKO male mice. Importantly, following TAC the dKO hearts showed low fibrosis levels, reduced inflammatory and hypertrophic gene expression and a significantly preserved cardiac function as compared with their WT counterparts in both genders. Consistent with these data, removing ATF3 resumed p38 activation in the JDP2 KO mice which correlates with the beneficial cardiac function. Collectively, mice with JDP2 and ATF3 double deficiency had reduced maladaptive cardiac remodeling and lower hypertrophy following TAC. As such, the worsening of the cardiac outcome found in the JDP2 KO mice is due to the elevated ATF3 expression. Simultaneous suppression of both ATF3 and JDP2 activity is highly beneficial for cardiac function in health and disease.
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