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The research team of Professor Jiang Qing from Nanjing University School of Medicine cooperated with the team of Professor Xue Bin of Shaw Hospital Affiliated to Nanjing Medical University, the team of Professor Li Chaojun of Nanjing Medical University, and the team of Professor Chen Di of Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences.
progress
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The research results, titled "Defects in a liver-bone axis contribute to hepatic osteodystrophy disease progression", were published online in "Cell Metabolism" on March 1, 2022 (Cell Metabolism)
Hepatic Osteodystrophy, also known as hepatic osteodystrophy, is a metabolic skeletal disease with an overall change in bone mineral density in patients with chronic liver injury, mostly caused by viral hepatitis, liver cirrhosis, and fatty liver
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The number of chronic liver injury patients worldwide has exceeded 840 million, and the number is increasing at a rate of 2 million per year
Osteoporosis Quality of Life
The collaborative team's research shows that there is an axial homeostatic regulation between the classical endocrine organ liver and the non-classical endocrine organ bone.
Once the homeostasis is disrupted, it will lead to the occurrence of hepatic bone disease
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The study found that the expression of the phosphatase PP2Acα in the liver was significantly increased in patients with clinical hepatic bone disease and in a mouse model
cholesterol
Fig.
This study not only revealed the important regulatory mechanism of the liver-bone axis in the progression of hepatic bone disease, but also provided a theoretical basis for the regulation of the interaction between organs, and provided a potential target for drug treatment of hepatic bone disease
Original source:
Lu K, Shi TS, Shen SY, Shi Y, Gao HL, Wu J, Lu X, Gao X, Ju HX, Wang W, Cao Y, Chen D, Li CJ, Xue B, Jiang Q.
Defects in a liver-bone axis contribute to hepatic osteodystrophy disease progression.
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