Abstract
Obesity and overweight are risk factors for the development of cardiovascular diseases. Importantly, cardiovascular diseases are the main cause of death worldwide, being responsible for around 31% of all deaths. Although initially thought as an energy storage tissue, adipose tissue is now recognized as an important endocrine organ. Adipose tissue communicates with other organs via hormones called adipokines, and as more recently demonstrated, via microRNAs (miRNAs). Our group has shown that the expression of DICER, an important protein involved in miRNAs processing, in adipose tissue, is altered in Obesity and aging. Indeed, adipose tissue-specific Dicer deletion in mice leads to insulin resistance, metabolic alterations in non-adipose tissues and premature aging. These data strongly evidence the crosstalk between adipose tissue and other organs via miRNAs. Cardiac tissue is able to use several different substrates; indeed, metabolic flexibility is closely associated with heart function. In addition, cardiac remodeling, as observed in hypertension, leads to alteration in cardiomyocyte metabolism. However, even with the well-established relationship between adipose tissue function and cardiovascular diseases, it is still not clear if miRNAs from adipose tissue play a role in cardiac function, whether in physiologic or pathologic scenarios. The aim of the present study is to investigate the crosstalk between adipose tissue and heart via miRNAs using an adipocyte-specific Dicer knockout mouse. Our hypothesis is that miRNAs from adipose tissue play a role in cardiac metabolism and function. Moreover, adipose tissue miRNAs could participate in cardiac remodeling during hypertension. (AU)
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