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Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1.

Authors: Xiao, Jinfeng  Jiang, Hong  Zhang, Rui  Fan, Guangpu  Zhang, Yan  Jiang, Dingsheng  Li, Hongliang 
Citation: Xiao J, etal., PLoS One. 2012;7(5):e35779. doi: 10.1371/journal.pone.0035779. Epub 2012 May 11.
Pubmed: (View Article at PubMed) PMID:22606234
DOI: Full-text: DOI:10.1371/journal.pone.0035779


BACKGROUND: Epidermal growth factor (EGF), latrophilin and seven transmembrane domain-containing protein 1 (ELTD1) is developmentally upregulated in the heart. Little is known about the relationship between ELTD1 and cardiac diseases. Therefore, we aimed to clarify the role of ELTD1 in pressure overload-induced cardiac hypertrophy.
METHODS AND RESULTS: C57BL/6J wild-type (WT) mice and ELTD1-knockout (KO) mice were subjected to left ventricular pressure overload by descending aortic banding (AB). KO mice exhibited more unfavorable cardiac remodeling than WT mice 28 days post AB; this remodeling was characterized by aggravated cardiomyocyte hypertrophy, thickening of the ventricular walls, dilated chambers, increased fibrosis, and blunted systolic and diastolic cardiac function. Analysis of signaling pathways revealed enhanced extracellular signal-regulated kinase (ERK) and the c-Jun amino-terminal kinase (JNK) phosphorylation in response to ELTD1 deletion.
CONCLUSIONS: ELTD1 deficiency exacerbates cardiac hypertrophy and cardiac function induced by AB-induced pressure overload by promoting both cardiomyocyte hypertrophy and cardiac fibrosis. These effects are suggested to originate from the activation of the ERK and JNK pathways, suggesting that ELTD1 is a potential target for therapies that prevent the development of cardiac disease.

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CRRD Object Information
CRRD ID: 13838662
Created: 2019-01-08
Species: All species
Last Modified: 2019-01-08
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.