From the Editor's Desk ...

被引:0
|
作者
Burra, Patrizia [1 ]
Tacke, Frank [2 ]
Ratziu, Vlad [3 ]
Zeuzem, Stefan [4 ]
Sangro, Bruno [5 ]
Angeli, Paolo [6 ]
机构
[1] Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, Padua, Italy
[2] Charite Univ Med Berlin, Dept Hepatol & Gastroenterol, Berlin, Germany
[3] Sorbonne Univ, Hosp Pitie Salpetriere, Insitute Cardiometab & Nutr, Paris, France
[4] Goethe Univ Hosp, Dept Med 1, Frankfurt, Germany
[5] Clin Univ Navarra, Liver Unit, CIBEREHD, Pamplona, Spain
[6] Univ Padua, Unit Internal Med & Hepatol, Padua, Italy
关键词
D O I
10.1016/j.jhep.2023.04.004
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
What a salty surprise: The magnesium transporter CNNM4 is a therapeutic target in NASH Hepatocyte homeostasis is severely disturbed in NASH, characterised by lipotoxicity, mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Simon and coworkers now demonstrate that this is accompanied by drastic changes in magnesium (Mg2+) homeostasis, because the Mg2+ transporter cyclin M4 (CNNM4) is upregulated in NASH and acts as a Mg2+ exporter in the liver. Using patient samples, primary hepatocyte cultures and rodent NASH models, downregulating CNNM4 in hepatocytes restored hepatic magnesium levels and reduced ER stress, which translated into improved steatosis, lower inflammation and reduced fibrosis. While these data indicate that
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页码:1 / 3
页数:3
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