Degrading NASH

Inflammation is one of the primary drivers of non-alcoholic steatohepatitis (NASH), but decreasing inflammation without creating susceptibility to infection remains a challenge for the field. In Nature Medicine this month, a Chinese team described how TMBIM1, a transmembrane regulator of vesicle trafficking, triggers breakdown of excess levels of a major inflammatory mediator of NASH when it is up-regulated during the disease, leaving normal levels of TLR4 to respond to infections.

NASH is a major complication of non-alcoholic fatty liver disease (NAFLD). As fat deposits accumulate in the liver -- a process known as steatosis --, some patients progress to full-blown NASH, developing chronic inflammation that ultimately leads to fibrosis. ...