Key result
Adipose HuR deletion triggers spontaneous cardiac hypertrophy and fibrosis via subcutaneous adipose inflammation.
Why the study?
Functional brown adipose tissue is known to associate with cardiovascular health, but the mechanisms by which brown adipose tissue function and adipose homeostasis directly mediate cardiovascular disease require clarification.
Does adipocyte-specific deletion of HuR induce cardiac hypertrophy and fibrosis in a preclinical model?
Does adipocyte-specific deletion of HuR induce cardiac hypertrophy and fibrosis in a preclinical model?
Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis, highlighting a potential mechanism by which brown adipose tissue function directly mediates cardiovascular disease.
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. These results may have implications on the mechanisms by which BAT function and adipose tissue homeostasis directly mediate cardiovascular disease.
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Guarnieri et al. (2021) studied Cardiac hypertrophy and fibrosis. Adipocyte-specific deletion of HuR vs. Littermate controls was evaluated on Development of cardiac hypertrophy and fibrosis. Adipose tissue-specific deletion of HuR induced the spontaneous development of cardiac hypertrophy and fibrosis in mice, driven by increased inflammatory gene expression in subcutaneous white adipose tissue.
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