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• W2788166883 abstract "We read with great interest the recently published paper by Kalfon, R and colleagues [ [1] Kalfon R. Haas T. Shofti R. et al. c-Jun dimerization protein 2 (JDP2) deficiency promotes cardiac hypertrophy and dysfunction in response to pressure overload. Int. J. Cardiol. 2017; 249: 357-363 Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar ]. They discovered involvements of JDP2 during TAC-caused cardiac remodeling, and suggested that JDP2-null mice suffered from deteriorated hypertrophy, fibrosis and malfunction as a result of ATF3 activation through limiting p38MAPK pathway. Consistently, by employing cardiomyocytes with isoprenaline infusion, Hill et al. gave insights that JDP2 overexpression was capable to blunt hypertrophic response due to specific abrogation of AP-1 [ [2] Hill C. Wurfel A. Heger J. et al. Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction. Cardiovasc. Res. 2013; 99: 121-128 Crossref PubMed Scopus (34) Google Scholar ]. Thus, JDP2 might serve as an appealing therapeutic target to reduce cardiac remodeling. Moreover, given importance of JDP2 as a potent repressor toward ATF3 [ [1] Kalfon R. Haas T. Shofti R. et al. c-Jun dimerization protein 2 (JDP2) deficiency promotes cardiac hypertrophy and dysfunction in response to pressure overload. Int. J. Cardiol. 2017; 249: 357-363 Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar ], it might confer promising avenues to clarify ATF3’ ambiguous roles in cardiac remodeling JDP2-associatedly. c-Jun dimerization protein 2 (JDP2) deficiency promotes cardiac hypertrophy and dysfunction in response to pressure overloadInternational Journal of CardiologyVol. 249PreviewThe c-Jun dimerization protein 2, JDP2, is a member of the basic leucine zipper (bZIP) superfamily [1]. JDP2 is constitutively expressed in all cells tested [2]. As a homodimer, JDP2 typically suppresses transcription through binding to CRE and TRE DNA elements found in the promoters of numerous genes by recruitment of histone deacetylases [3]. Alternatively, JDP2 associates with other members of the bZIP family. JDP2 is able to activate transcription when associated with CHOP10 [4] or as a co-activator of the steroid hormone receptors [5]. Full-Text PDF JDP2 and ATF3 — bZIP repressors in cardiac remodelingInternational Journal of CardiologyVol. 257PreviewWe thank Guo et al. for their letter to the editor entitled “JDP2: A novel therapeutic thought in cardiac remodeling”. JDP2 and ATF3 are two basic leucine zipper protein (bZIP) members of the AP-1 family of transcription factors. JDP2 and ATF3 share a high degree of homology within their bZIP domain and bind related TPA- and cAMP-response elements found in the promoter of numerous genes. JDP2 and ATF3 possess indistinguishable transcription repression activity [1]. ATF3 was found to be elevated in patients with heart failure [2], however, whether the expression of ATF3 is adaptive or maladaptive is currently unknown. Full-Text PDF" @default.
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• W2788166883 date "2018-04-01" @default.
• W2788166883 modified "2023-10-18" @default.
• W2788166883 title "JDP2: A novel therapeutic thought in cardiac remodeling" @default.
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• W2788166883 doi "https://doi.org/10.1016/j.ijcard.2017.09.210" @default.
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