Cardiac-specific deletion of SOCS-3 prevents development of left ventricular remodeling after acute myocardial infarction.

Journal of the American College of Cardiology
Toyoharu ObaTsutomu Imaizumi

Abstract

The study investigated the role of myocardial suppressor of cytokine signaling-3 (SOCS3), an intrinsic negative feedback regulator of the janus kinase and signal transducer and activator of transcription (JAK-STAT) signaling pathway, in the development of left ventricular (LV) remodeling after acute myocardial infarction (AMI). LV remodeling after AMI results in poor cardiac performance leading to heart failure. Although it has been shown that JAK-STAT-activating cytokines prevent LV remodeling after AMI in animals, little is known about the role of SOCS3 in this process. Cardiac-specific SOCS3 knockout mice (SOCS3-CKO) were generated and subjected to AMI induced by permanent ligation of the left anterior descending coronary artery. Although the initial infarct size after coronary occlusion measured by triphenyltetrazolium chloride staining was comparable between SOCS3-CKO and control mice, the infarct size 14 days after AMI was remarkably inhibited in SOCS3-CKO, indicating that progression of LV remodeling after AMI was prevented in SOCS3-CKO hearts. Prompt and marked up-regulations of multiple JAK-STAT-activating cytokines including leukemia inhibitory factor and granulocyte colony-stimulating factor (G-CSF) were observed wit...Continue Reading

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Citations

Feb 1, 2013·Hypertension Research : Official Journal of the Japanese Society of Hypertension·Fouad A ZoueinGeorge W Booz
Jul 6, 2012·Hypertension Research : Official Journal of the Japanese Society of Hypertension·Haruya OhmuraTsutomu Imaizumi
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Feb 16, 2021·Frontiers in Cell and Developmental Biology·Shuang LiuBo Zhang

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