Yong-Xu Wang
University of Massachusetts Chan Medical School, MA·Physiology
Fat building up inside liver cells can trigger a serious disease. In nonalcoholic steatohepatitis (NASH), lipid accumulation in liver cells (steatosis) is followed by inflammation, swollen "ballooned" cells and scarring (fibrosis).
- Fields
Physiology
Biochemistry
Medicine & Clinical Research
- Topics
nonalcoholic steatohepatitis
nonalcoholic fatty liver disease
hepatic steatosis
- Grants
- 1 known grant, through Jun 2028
What they work on
- Test whether a newly identified adipokine, a hormone released by fat tissue, resolves NASH and associated metabolic problems in two different NASH mouse models.
- Determine the in vivo mechanism by which the adipokine clears liver fat, focusing on its effects on mitochondrial biogenesis, fatty acid oxidation and de novo lipogenesis gene programs in mouse liver.
- Identify the cell-surface receptor that the adipokine acts through and map its downstream signaling using global phosphoproteomics, which profiles protein phosphorylation across the cell.
More about the research
The disease can progress to cirrhosis, liver failure and cancer. It is common worldwide, yet there are no approved therapies. Because fat buildup is a key driver of NASH, finding natural signals that control how the liver handles fat could open new treatment routes.
Why it matters
NASH is a widespread liver disease that can lead to cirrhosis, liver failure and cancer, and patients currently have no FDA-approved therapy. This work tests whether a fat-tissue hormone that drives the liver to burn rather than make fat could serve as a therapeutic agent. Identifying its receptor and signaling pathway could also point to new drug targets for NASH and related metabolic diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Nicholas Davidson
Washington University in St Louis, MO·Medicine & Clinical Research
Determine how the human TM6SF2 E167K variant alters fat loading onto APOB and the release of VLDL from the liver and chylomicrons from the gut, using liver-specific knockout and variant knock-in mice.
Ren Zhang
Wayne State University, MI·Biochemistry
Determine whether MNADK, the mitochondrial NAD kinase, preserves liver energy balance and insulin sensitivity and reduces risk of NASH and type 2 diabetes, using genetically engineered mouse models.
John Clarke
Washington State University, WA·Pharmacology
Define which protein phosphatase 2A-associated pathways mediate microcystin-LR effects on human HepaRG hepatocytes and LX2 stellate cells, the liver's scar-forming cells, co-cultured as 3D spheroids in static and microfluidic systems with pathway modulators.
The school
University of Massachusetts Chan Medical School: 29 labs on PI Pages, $350M a year on research, 55 research doctorates a year.
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