Xiaolei Liu
Temple University, PA·Physiology
Heart attacks, or myocardial infarctions (MI), are a leading cause of illness and death worldwide, and new ways to help the heart heal are still needed. The lymphatic system is a network of vessels that drains fluid and carries immune cells.
- Fields
Physiology
Medicine & Clinical Research
Biology
- Topics
cardiac lymphatics
lymphangiogenesis
lymphatic endothelial cells
- Grants
- 1 known grant, through Dec 2027
What they work on
- Determine the molecular pathways and targets through which lymphatic growth in the heart improves cardiomyocyte survival after myocardial infarction, building on survival signals such as Reelin released by lymphatic endothelial cells.
- Characterize how lymphatic vessels support heart repair, including immune cell clearance, using mouse strains with reduced or increased lymphatic function after MI.
- Test whether enhancing heart lymphatic functions in mouse models has therapeutic potential for treating ischemic heart disease.
More about the research
Earlier studies found that growing more lymphatic vessels in the heart after injury improves heart function and limits harmful remodeling, probably by clearing inflammation. The PI's published work added another role. Lymphatic endothelial cells, the cells that line these vessels, release Reelin, a signal that helps heart muscle cells survive. This challenges the view that lymphatics are only passive drainage pipes.
Why it matters
Heart failure after heart attack remains a major cause of death. By showing how heart lymphatic vessels protect heart muscle cells and clear inflammation after injury, this work could identify new treatment targets, such as lymphatic-derived survival signals, to improve recovery for patients with ischemic heart disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Joseph Hill
University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research
Determine how endothelial Fli1 protects the heart under ischemic stress, using tamoxifen-inducible mice that lack Fli1 only in blood vessel lining cells, and manipulate Fli1 activity in models of ischemic heart disease.
Shah Ali
Columbia University, NY·Medicine & Clinical Research
Build a genetic mouse model in which the biotin-tagging enzyme TurboID sits in the endoplasmic reticulum of cardiac fibroblasts, so the proteins these scar-forming cells secrete can be labeled in living animals.
Bradford Hill
University of Louisville, KY·Physiology
Determine how alternative splicing of Pkm, which switches fibroblasts between the slower Pkm2 and faster Pkm1 enzyme forms, changes cardiac fibroblast metabolism and the amount of fibrosis after myocardial infarction.
The school
Temple University: 22 labs on PI Pages, $315M a year on research, 238 research doctorates a year.
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