Shuxia Wang
University of Kentucky, KY·Medicine & Clinical Research
Obesity raises the risk of non-alcoholic fatty liver disease (NAFLD), in which fat builds up in the liver. NAFLD can progress to non-alcoholic steatohepatitis (NASH), a more damaging form with inflammation.
- Fields
Medicine & Clinical Research
Physiology
Microbiology & Immunology
- Topics
non-alcoholic fatty liver disease
non-alcoholic steatohepatitis
obesity
- Grants
- 1 known grant, through Apr 2027
What they work on
- Determine how the macrophage protein SMPDL3B regulates the receptor CD36 and the inflammatory signaling triggered when TSP1, a signaling protein, binds CD36.
- Establish the role of macrophage SMPDL3B in the development and progression of obesity-associated fatty liver disease, using animal models and lab-grown human liver organoids.
- Test whether a peptide nanoparticle conjugate that blocks TSP1–CD36 binding restores liver macrophage SMPDL3B and reduces liver inflammation and NAFLD/NASH progression in obese animals.
More about the research
As obesity becomes more common, NAFLD is rising, and there are few treatment options. A key question is why immune cells in the liver turn inflammatory in obesity and push the disease forward.
Why it matters
NAFLD is becoming one of the most common liver diseases worldwide, driven by obesity and metabolic disease. Clarifying how liver macrophages become inflammatory could identify new treatment strategies for obesity-associated NAFLD and NASH. Testing a peptide nanoparticle that blocks TSP1–CD36 binding in animals is a step toward a possible therapy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hongxue Shi
Louisiana State University Health Sciences Center-Shreveport, LA·Medicine & Clinical Research·Early-career
Test whether loss of TIM4, a macrophage receptor that captures apoptotic cells, impairs clearance of dying liver cells and speeds NASH fibrosis, by deleting or restoring macrophage TIM4 in NASH 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.
James Hahn
George Washington University, DC·Biomedical Engineering
Develop machine learning algorithms that predict liver fat (hepatic steatosis), liver scarring (fibrosis), body fat and blood biomarkers from 3D optical body surface scans, trained and validated against liver biopsy data.
The school
University of Kentucky: 34 labs on PI Pages, $528M a year on research, 319 research doctorates a year.
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