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Cells 2014, 3(3), 702-712; doi:10.3390/cells3030702

MicroRNAs Control Macrophage Formation and Activation: The Inflammatory Link between Obesity and Cardiovascular Diseases

1
Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX 77843, USA
2
Department of Animal Science, Texas A&M University, College Station, TX 77843, USA
These authors contributed equally to this article.
*
Author to whom correspondence should be addressed.
Received: 29 May 2014 / Revised: 27 June 2014 / Accepted: 1 July 2014 / Published: 10 July 2014
(This article belongs to the Special Issue MicroRNAs in Cardiovascular Biology and Disease)
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Abstract

Activation and recruitment of resident macrophages in tissues in response to physiological stress are crucial regulatory processes in promoting the development of obesity-associated metabolic disorders and cardiovascular diseases. Recent studies have provided compelling evidence that microRNAs play important roles in modulating monocyte formation, macrophage maturation, infiltration into tissues and activation. Macrophage-dependent systemic physiological and tissue-specific responses also involve cell-cell interactions between macrophages and host tissue niche cell components, including other tissue-resident immune cell lineages, adipocytes, vascular smooth muscle and others. In this review, we highlight the roles of microRNAs in regulating the development and function of macrophages in the context of obesity, which could provide insights into the pathogenesis of obesity-related metabolic syndrome and cardiovascular diseases. View Full-Text
Keywords: microRNA; macrophage; obesity; cardiovascular diseases microRNA; macrophage; obesity; cardiovascular diseases
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Chang, R.C.-A.; Ying, W.; Bazer, F.W.; Zhou, B. MicroRNAs Control Macrophage Formation and Activation: The Inflammatory Link between Obesity and Cardiovascular Diseases. Cells 2014, 3, 702-712.

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