Abstract
Hepatic osteodystrophy (HOD) is a metabolic bone disease caused by chronic liver injuries and complicated with osteopenia or osteoporosis. Here, we identified LCAT as a hepatokine, regulated by PP2Acα, which prevents bone loss, as well as ameliorates chronic liver injury. Conversely, loss of function of LCAT markedly exacerbated the bone loss phenotype of HOD. Mechanistically, we found that LCAT activation is mediated by PP2Acα/USF1 signaling and demonstrated that alteration of the cholesterol levels is involved in the regulation of osteoblast and osteoclast activities. Additionally, LCAT improves the liver fibrosis and liver function by reversing cholesterol transport in HOD. In summary, we discovered that PP2A-regulated hepatokine LCAT controls HOD by maintaining the balance of the liver-bone axis.
Published Version
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