Hongxue Shi
Louisiana State University Health Sciences Center-Shreveport, LA·Medicine & Clinical Research·Early-career
Non-alcoholic steatohepatitis (NASH) is the most common cause of chronic liver disease. It is driven by rising rates of obesity and diabetes, and there are still no FDA-approved drugs to treat it.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Physiology
- Topics
non-alcoholic steatohepatitis
fatty liver disease
liver fibrosis
- Grants
- 1 known grant, through Jul 2028
What they work on
- 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.
- Test a mechanism-based drug strategy to restore macrophage TIM4 in NASH mice, and use single-cell RNA sequencing to find macrophage signals that keep scar-forming hepatic stellate cells inactive.
- Test whether blocking SIRPα, part of a "don't eat me" signal, while silencing liver-cell TAZ reduces fibrotic NASH, using complementary mouse models.
- Identify macrophage-secreted proteins induced by eating necroptotic liver cells that lower TAZ, using a secretome mouse model and proteomics, and define how TREM2 and LRP1 contribute.
More about the research
In NASH, dead liver cells (hepatocytes) pile up. Normally, immune cells called macrophages clear away dead cells safely. This project asks why that cleanup fails in NASH and whether fixing it can slow liver scarring, called fibrosis.
Why it matters
NASH affects many people with obesity and diabetes, and there are no approved drugs. Showing how macrophage cleanup of dead liver cells fails, and how restoring it with targets such as TIM4, SIRPα or TAZ might curb fibrosis, could point to new treatment strategies for patients with fibrotic NASH.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Tatiana Kisseleva
University of Southern California, CA·Medicine & Clinical Research
Identify genes that are more active in hepatic stellate cells (the liver's scar-forming cells) from human AALD livers than in normal, NAFL or NASH livers, using single-nucleus RNA sequencing (snRNA-seq).
Shuxia Wang
University of Kentucky, KY·Medicine & Clinical Research
Determine how the macrophage protein SMPDL3B regulates the receptor CD36 and the inflammatory signaling triggered when TSP1, a signaling protein, binds CD36.
Jennifer Chen
University of California-San Francisco, CA·Medicine & Clinical Research
Determine how ceramide inhibits YAP/TAZ, signaling proteins of the Hippo growth-control pathway, in hepatic stellate cells, using gain- and loss-of-function experiments and mice lacking acid ceramidase in these cells.
The school
Louisiana State University Health Sciences Center-Shreveport: 6 labs on PI Pages, $32M a year on research, 9 research doctorates a year.
More about Louisiana State University Health Sciences Center-Shreveport
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