Key result
ELTD1 deficiency exacerbates cardiac hypertrophy, increasing fibrosis area ~65% after pressure overload in mice.
Why the study?
The role of ELTD1 in pressure overload-induced cardiac hypertrophy and cardiac diseases was unclear.
Does ELTD1 deficiency exacerbate cardiac hypertrophy and dysfunction in response to pressure overload in mice?
Does ELTD1 deficiency exacerbate cardiac hypertrophy and dysfunction in response to pressure overload in mice?
ELTD1 deficiency exacerbates pressure overload-induced cardiac hypertrophy and dysfunction in mice, suggesting ELTD1 as a potential therapeutic target for cardiac disease.
Answers are grounded in this paper and cite their sources.
ELTD1 deficiency exacerbates pressure overload hypertrophy and fibrosis in mice; hypothesis-generating for ELTD1 modulation in human cardiac remodeling.
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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Xiao et al. (2012) studied Cardiac hypertrophy (n=75). ELTD1 deficiency vs. Wild-type mice was evaluated on Cardiac hypertrophy and remodeling (HW/BW ratio, cardiomyocyte cross-sectional area, fibrosis, and cardiac function) (p=<0.01). ELTD1 deficiency exacerbated pressure overload-induced cardiac hypertrophy in mice, leading to an approximately 27% greater increase in heart weight to body weight ratio and 65% greater increase in fibrosis area compared to wild-type mice.
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