The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodelling
The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodelling
Atherosclerosis: Open Access (Omics Publishing S.L) has announced almost 50 % discount on article processing charge to commemorate its 10th Anniversary.
Atherosclerosis: Open Access is an open access, peer-reviewed journal that focuses and welcomes submissions on all aspects of Coronary Heart disease, Stroke, Peripheral Arterial Disease, Chronic Kidney Disease, arteriosclerosis, Coronary Atherosclerosis, intracranial atherosclerosis etc.
It gives us great pleasure to announce the call for paper on the occasion of 10th Anniversary of the Journal at special and hefty discount of up to 50 % on one-time article processing charge. Prospective academicians and scientists are encouraged to utilize this opportunity to get their articles reviewed, processed and published at relatively faster pace and at lower charges. In addition to this, the authors who publish with us during the year-long celebrations will also be eligible for academic awards recommended by the editorial panel.
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Title: “The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodelling”
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.
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Atherosclerosis: Open Access