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Augmented Cardiac Hypertrophy in Response to Pressure Overload in Mice Lacking ELTD1

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单位: [1]Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430072, Peoples R China [2]Wuhan Univ, Cardiovasc Res Inst, Wuhan 430072, Peoples R China [3]Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Thorac & Cardiac Surg, Wuhan 430074, Peoples R China
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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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出版当年[2011]版:
大类 | 2 区 生物
小类 | 2 区 生物学
最新[2025]版:
大类 | 3 区 综合性期刊
小类 | 3 区 综合性期刊
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出版当年[2010]版:
Q1 BIOLOGY
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Q2 MULTIDISCIPLINARY SCIENCES

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第一作者单位: [1]Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430072, Peoples R China [2]Wuhan Univ, Cardiovasc Res Inst, Wuhan 430072, Peoples R China
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通讯机构: [1]Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430072, Peoples R China [2]Wuhan Univ, Cardiovasc Res Inst, Wuhan 430072, Peoples R China
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