Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis

The presence of functional brown adipose tissue in humans is known to be associated with cardiovascular health. Here, we show that adipocyte-specific deletion of the RNA binding protein HuR, which we have previously shown to reduce BAT-mediated thermogenesis, is sufficient to mediate a spontaneous development of cardiac hypertrophy and fibrosis, likely through increased inflammation and extracellular vesicle transport in subcutaneous white adipose tissue. These results may have implications on the mechanisms by which BAT function and adipose tissue homeostasis directly mediates CVD. RNA-seq to determine global gene expression profiles cardiac and subcutaneous white adipose samples from mice with adipocyte-specific HuR gene deletion.