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The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling. | OMICS International| Abstract

Atherosclerosis: Open Access
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  • Atheroscler Open Access 2016, Vol 1(1): 101

The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling.

Zhi-Ping Liu*
Department of Internal Medicine Cardiology, UT Southwestern Medical Center, , 6000 Harry Hines Blvd Dallas, Texas 75390, United States
*Corresponding Author : Zhi-Ping Liu, Department of Internal Medicine Cardiology, UT Southwestern Medical Center, 6000 Harry Hines Blvd Dallas, Texas 75390, United States, Tel: 214-648-1485, Email: [email protected]

Received Date: Oct 12, 2015 / Accepted Date: Nov 12, 2015 / Published Date: Nov 19, 2015

Abstract

Inflammation in post-myocardial infarct (MI) is necessary for myocyte repair and wound healing. Unfortunately it is also a key component of adverse post-myocardial infarction (MI) left ventricular (LV) remodeling that can lead to heart failure. FoxO4 has pleiotropic cell-type and context-dependent functions involved in a variety of human diseases. Recently, we identified a novel function of FoxO4 in post-MI LV remodeling. FoxO4 promotes early post-MI inflammatory response via endothelial Arginase 1 (Arg1). FoxO4 can activate the transcription of endothelial Arg1 in response to ischemia, leading to decreased nitric oxide production and enhanced monocyte adhesion and transmigration through endothelial barrier. Inactivation of FoxO4 resulted in attenuated post-MI inflammation and better preserved cardiac function compared to WT mice. FoxO4 could be a potential therapeutic target in post-MI heart repair and regeneration.

Citation: Liu ZP (2015) The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling. Atheroscler open access 1: 101.

Copyright: © 2015 Liu ZP. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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