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.已知人类体内功能性棕色脂肪组织（brown adipose tissue，BAT）的存在与心血管健康密切相关。本研究证实，脂肪细胞特异性敲除RNA结合蛋白HuR（前期研究已表明该蛋白可降低BAT介导的产热功能）可自发诱发心脏肥大与纤维化，其潜在机制可能与皮下白色脂肪组织内炎症水平升高及细胞外囊泡运输增强相关。上述结果可为阐明BAT功能与脂肪组织稳态直接介导心血管疾病（cardiovascular disease，CVD）的潜在机制提供参考。本研究通过RNA测序（RNA-seq）对脂肪细胞特异性HuR基因敲除小鼠的心脏及皮下白色脂肪组织样本开展了全基因表达谱分析。