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Nathan L. Priceab, Cristina M. Ramírezab & Carlos Fernández-Hernando*aba Vascular Biology and Therapeutics Programb Integrative Cell Signaling and Neurobiology of Metabolism Program, Section of Comparative Medicine, Yale University School of Medicine New Haven, CTUSAReferee: Dr. Katey Rayner, Director, Cardiometabolic microRNA and Epigenetics Laboratory, University of Ottawa Heart Institute and Assistant Professor, University of Ottawa, Ottawa, Ontario, Canada.Address for correspondence: Carlos Fernández-Hernando, PhDVascular Biology and Therapeutics Program, Yale University School of Medicine 10 Amistad Street, Amistad Research Building, Room 337C, New Haven, CT 06510USA. Tel: +203 737 4615. Fax: +203 737 2290. E-mail: carlos.fernandez@yale.eduAbstractMetabolic syndrome is a complex metabolic condition caused by abnormal adipose deposition and function, dyslipidemia and hyperglycemia, which affects >47 million American adults and ∼1 million children. Individuals with the metabolic syndrome have essentially twice the risk for developing cardiovascular disease (CVD) and Type 2 diabetes mellitus (T2D), compared to those without the syndrome. In the search for improved and novel therapeutic strategies, microRNAs (miRNA) have been shown to be interesting targets due to their regulatory role on gene networks controlling different crucial aspects of metabolism, including lipid and glucose homeostasis. More recently, the discovery of circulating miRNAs suggest that miRNAs may be involved in facilitating metabolic crosstalk between organs as well as serving as novel biomarkers of diseases, including T2D and atherosclerosis. These findings highlight the importance of miRNAs for regulating pathways that underlie metabolic diseases, and their potential as therapeutic targets for the development of novel treatments.
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