Jennifer Chen
University of California-San Francisco, CA·Medicine & Clinical Research
Chronic liver diseases share a common, dangerous endpoint: fibrosis, or scarring. Scarring builds up when the body lays down more extracellular matrix (ECM), the protein scaffolding between cells, than it breaks down.
- Fields
Medicine & Clinical Research
Biochemistry
Physiology
- Topics
liver fibrosis
hepatic fibrosis
chronic liver disease
- Grants
- 2 known grants, through May 2028
What they work on
- 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.
- Characterize how ceramide regulates remodeling of the extracellular matrix, the scar-forming protein scaffold, in liver fibrosis, using cultured cells and HSC-specific knockout mice.
- Test whether the Ceramide Responsiveness Score, a gene signature, tracks fibrosis stage, progression and clinical features in deidentified human liver samples.
More about the research
Over time, fibrosis can lead to liver failure. There are no FDA-approved drugs that target fibrosis, and few biomarkers show which disease processes are active in an individual patient. This research seeks antifibrotic therapies and biomarkers that could identify the patients most likely to benefit from them.
Why it matters
Fibrosis drives liver failure in chronic liver disease, and no approved therapies target it. Understanding how ceramide calms scar-forming liver cells could reveal new drug targets. Validating the Ceramide Responsiveness Score could support a personalized-medicine approach, helping doctors identify which patients with liver fibrosis are most likely to benefit from future antifibrotic treatments.
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).
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.
Zhongkui Hong
Texas Tech University, TX·Biomedical Engineering
Define how stiffness and composition of the extracellular matrix control adhesion and migration of vascular smooth muscle cells through YAP/TAZ mechanotransduction, using cells from ApoE⁻/⁻ mice.
The school
University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.
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