Wendy Liu
Stanford University, CA·Neuroscience·Early-career
Vision depends on retinal ganglion cells, the neurons whose long fibers form the optic nerve and carry visual signals from the eye to the brain. When these cells die, as they do in glaucoma and after optic nerve injury, sight is lost permanently.
- Fields
Neuroscience
Biomedical Engineering
Medicine & Clinical Research
- Topics
retinal ganglion cells
glaucoma
intraocular pressure
- Grants
- 2 known grants, through Aug 2028
What they work on
- Determine which ultrasound parameters effectively stimulate retinal ganglion cells in the living eye, using a transparent ultrasound transducer together with two-photon calcium imaging of genetically encoded calcium indicators in animal models.
- Test the biophysical mechanisms by which ultrasound alters retinal neuron activity in vivo, and evaluate its therapeutic efficacy for protecting retinal ganglion cells after optic nerve injury.
- Measure the contribution of mechanosensitive ion channels, which open when cells are physically deformed, to pressure-activated electrical currents in retinal cells subjected to mechanical stimulation in vitro.
- Test how human genetic variants in mechanosensitive ion channel genes associated with glaucoma risk change channel function, by expressing the variant channels in a heterologous cell system.
- Test whether mechanosensitive ion channels mediate retinal ganglion cell death in a mouse model of glaucoma, linking intraocular pressure sensing to neuron loss.
More about the research
Two linked questions drive the research here: how physical forces in the eye, especially pressure, are sensed by retinal cells and can kill these neurons, and how a different physical input, focused ultrasound, can be used deliberately to stimulate and protect them. Both projects treat the retina as a tissue that responds to mechanical stimuli, and both work toward treatments for blinding optic nerve disease.
Why it matters
Glaucoma is a common, progressive cause of blindness, and no treatment directly addresses how the eye senses the pressure that damages it. Identifying the pressure-sensing ion channels that drive retinal ganglion cell death, and the gene variants that raise risk, could reveal targets for neuroprotective drugs. In parallel, understanding how ultrasound stimulates these same neurons could support safer, noninvasive ultrasound therapies for optic nerve disorders and retinal degeneration.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Raghu Krishnamoorthy
University of North Texas Health Science Center, TX·Pharmacology
Determine whether endothelin-1 (ET-1), a blood-vessel-tightening protein, acts through its ETA and ETB receptors to reduce mitophagy, the removal of damaged mitochondria, in retinal ganglion cells.
Karsten Gronert
University of California-Berkeley, CA·Neuroscience
Define which retinal cells make and respond to prostaglandin D2 (PGD2), a fat-derived signaling molecule, in healthy retina and how raised eye pressure (ocular hypertension) shuts this pathway down.
Matthew Veldman
Medical College of Wisconsin, WI·Neuroscience
Determine when srebf2, a master regulator of cholesterol production, is needed in zebrafish retinal ganglion cells for optic nerve regeneration, using srebf2 activity reporter lines.
The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
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