Bio


Dr. Wendy Liu, MD, PhD, is a fellowship-trained glaucoma and cataract surgeon. Her clinical practice focuses on management of adult glaucoma and cataracts. She specializes in traditional glaucoma surgery as well as minimally-invasive glaucoma surgery, such as iStent, Hydrus, Xen, KDB, OMNI, and GATT. Her goal is to work together with patients to determine what the best treatment options are for them, so they can maintain the best vision and quality of life.

In addition to clinical practice, Dr. Liu engages in translational research with the goal of finding new druggable targets in glaucoma treatment. Her interests include the role of mechanosensation in the eye as it relates to the pathophysiology of glaucoma.

Dr. Liu graduated summa cum laude from Princeton University with a degree in Molecular Biology and certificates in biophysics, materials science and engineering. She received several awards for excellence in academics and research, including the Shapiro Award for Academic Excellence, the American Society for Microbiology Undergraduate Research Fellowship, and the Sigma Xi Book Award for the best senior thesis. She subsequently earned her MD with honors from Harvard Medical School in the Harvard-MIT Program in Health Sciences and Technology, and PhD in Neurobiology from Harvard University. At Harvard, she was awarded the Presidential Scholarship and Martha Gray Prize for Excellence in Research. She was selected to receive a Howard Hughes Medical Institute research fellowship for her PhD work, which led to the discovery of novel thermosensory and olfactory circuits in the fruit fly using in vivo electrophysiology. She completed her ophthalmology residency at Massachusetts Eye and Ear, where she was awarded the Gragoudas Folkman Award for the best research grant proposal. She completed her glaucoma fellowship at Wills Eye Hospital.

Dr. Liu has published first-author articles in journals including New England Journal of Medicine, Nature, Proceedings of the National Academy of Sciences, and Current Biology. She is a member of the American Academy of Ophthalmology, the Association for Research in Vision and Ophthalmology, and the American Glaucoma Society.

Clinical Focus


  • Ophthalmology
  • Glaucoma
  • Cataracts
  • Minimally Invasive Surgical Procedures

Academic Appointments


Honors & Awards


  • Heed Ophthalmic Foundation Residents Retreat, Heed Ophthalmic Foundation
  • Gragoudas-Folkman Award, Massachusetts Eye and Ear
  • Martha Gray Prize for Excellence in Research, Harvard Medical School
  • Presidential Scholarship, Harvard Medical School
  • International Student Research Fellowship, Howard Hughes Medical Institute
  • Graduated Summa Cum Laude with Highest Honors in Molecular Biology, Princeton University
  • Certificates in Biophysics, Materials Science and Engineering, Princeton University
  • George Khoury ’65 Prize for Academic Excellence, Princeton University
  • Sigma Xi Book Award for best senior thesis in Molecular Biology, Princeton University
  • Phi Beta Kappa, Princeton University
  • Sigma Xi, Princeton University

Professional Education


  • Fellowship, Wills Eye Hospital, Glaucoma
  • Residency, Massachusetts Eye and Ear, Ophthalmology
  • Internship, Beth Israel Deaconess Medical Center, Internal Medicine
  • MD, Harvard Medical School, Medicine
  • PhD, Harvard University, Neurobiology
  • AB, Princeton University, Molecular Biology

Current Research and Scholarly Interests


Dr. Liu's research interests include the role of mechanosensation in the eye as it relates to the pathophysiology of glaucoma, with the goal of finding new druggable targets in glaucoma treatment.

Questions we are interested in studying include:
1) What are the ion channels that mediate pressure sensing in the eye?
2) What physiological roles do these channels play in the eye?
3) How do these ion channels mediate the development of ocular pathologies?

We study these questions using a combination of techniques including patch clamp electrophysiology, molecular biology, human genetics, and animal models of glaucoma and other ocular diseases.

** We are currently looking for postdoctoral fellows and researchers to join our group. Highly motivated candidates with expertise in techniques such as eye and brain histology, molecular and cellular biology, patch clamp electrophysiology, calcium imaging and animal handling experience are encouraged to apply.

Requirements: Completion of PhD, MD, or MD PhD training. Previous experience in vision or neuroscience research is ideal.

How to Apply: Please send a copy of your CV (please include list of publications, research skills, and contact for 3 references) to: Dr. Wendy Liu wendywliu@stanford.edu **

All Publications


  • Repair of Tube Erosion by Modifying the Tube Extender JOURNAL OF GLAUCOMA Liu, W. W., Werner, A., Chen, T. C. 2020; 29 (7): 604-606

    Abstract

    We describe here a case report of a novel technique for tube erosion repair, which modifies and utilizes the commercially available tube extender (Model TE). The modification of the tube extender makes the commercially available tube extender more compact and is useful in cases where conjunctival mobility and space are limited. This debulking of the tube extender may reduce the risk of future tube exposure and dellen formation.

    View details for DOI 10.1097/IJG.0000000000001505

    View details for Web of Science ID 000559090500025

    View details for PubMedID 32251073

    View details for PubMedCentralID PMC7337120

  • Three-dimensional Neuroretinal Rim Thickness and Visual Fields in Glaucoma: A Broken-stick Model. Journal of glaucoma Liu, W. W., McClurkin, M., Tsikata, E., Hui, P. C., Elze, T., Celebi, A. R., Khoueir, Z., Lee, R., Shieh, E., Simavli, H., Que, C., Guo, R., de Boer, J., Chen, T. C. 2020; 29 (10): 952-963

    Abstract

    In open-angle glaucoma, when neuroretinal rim tissue measured by volumetric optical coherence tomography (OCT) scans is below a third of the normal value, visual field (VF) damage becomes detectable.To determine the amount of neuroretinal rim tissue thickness below which VF damage becomes detectable.In a retrospective cross-sectional study, 1 eye per subject (of 57 healthy and 100 open-angle glaucoma patients) at an academic institution had eye examinations, VF testing, spectral-domain OCT retinal nerve fiber layer (RNFL) thickness measurements, and optic nerve volumetric scans. Using custom algorithms, the minimum distance band (MDB) neuroretinal rim thickness was calculated from optic nerve scans. "Broken-stick" regression was performed for estimating both the MDB and RNFL thickness tipping-point thresholds, below which were associated with initial VF defects in the decibel scale. The slopes for the structure-function relationship above and below the thresholds were computed. Smoothing curves of the MDB and RNFL thickness covariates were evaluated to examine the consistency of the independently identified tipping-point pairs.Plots of VF total deviation against MDB thickness revealed plateaus of VF total deviation unrelated to MDB thickness. Below the thresholds, VF total deviation decreased with MDB thickness, with the associated slopes significantly greater than those above the thresholds (P<0.014). Below 31% of global MDB thickness, and 36.8% and 43.6% of superior and inferior MDB thickness, VF damage becomes detectable. The MDB and RNFL tipping points were in good accordance with the correlation of the MDB and RNFL thickness covariates.When neuroretinal rim tissue, characterized by MDB thickness in OCT, is below a third of the normal value, VF damage in the decibel scale becomes detectable.

    View details for DOI 10.1097/IJG.0000000000001604

    View details for PubMedID 32925518

    View details for PubMedCentralID PMC7541591

  • Imaging Retinal Ganglion Cell Death and Dysfunction in Glaucoma. International ophthalmology clinics Liu, W. W., Margeta, M. A. 2019; 59 (4): 41-54

    View details for DOI 10.1097/IIO.0000000000000285

    View details for PubMedID 31569133

  • Diagnosing Myasthenia Gravis with an Ice Pack NEW ENGLAND JOURNAL OF MEDICINE Liu, W. W., Chen, A. 2016; 375 (19): E39

    View details for DOI 10.1056/NEJMicm1509523

    View details for Web of Science ID 000387534200001

    View details for PubMedID 27959645

  • Thermosensory processing in the Drosophila brain NATURE Liu, W. W., Mazor, O., Wilson, R. I. 2015; 519 (7543): 353-+

    Abstract

    In Drosophila, just as in vertebrates, changes in external temperature are encoded by bidirectional opponent thermoreceptor cells: some cells are excited by warming and inhibited by cooling, whereas others are excited by cooling and inhibited by warming. The central circuits that process these signals are not understood. In Drosophila, a specific brain region receives input from thermoreceptor cells. Here we show that distinct genetically identified projection neurons (PNs) in this brain region are excited by cooling, warming, or both. The PNs excited by cooling receive mainly feed-forward excitation from cool thermoreceptors. In contrast, the PNs excited by warming ('warm-PNs') receive both excitation from warm thermoreceptors and crossover inhibition from cool thermoreceptors through inhibitory interneurons. Notably, this crossover inhibition elicits warming-evoked excitation, because warming suppresses tonic activity in cool thermoreceptors. This in turn disinhibits warm-PNs and sums with feed-forward excitation evoked by warming. Crossover inhibition could cancel non-thermal activity (noise) that is positively correlated among warm and cool thermoreceptor cells, while reinforcing thermal activity which is anti-correlated. Our results show how central circuits can combine signals from bidirectional opponent neurons to construct sensitive and robust neural codes.

    View details for DOI 10.1038/nature14170

    View details for Web of Science ID 000351171900041

    View details for PubMedID 25739502

    View details for PubMedCentralID PMC5488797

  • Transient and Specific Inactivation of Drosophila Neurons In Vivo Using a Native Ligand-Gated Ion Channel CURRENT BIOLOGY Liu, W. W., Wilson, R. I. 2013; 23 (13): 1202-1208

    Abstract

    A key tool in neuroscience is the ability to transiently inactivate specific neurons on timescales of milliseconds to minutes. In Drosophila, there are two available techniques for accomplishing this (shibire(ts) and halorhodopsin [1-3]), but both have shortcomings [4-9]. Here we describe a complementary technique using a native histamine-gated chloride channel (Ort). Ort is the receptor at the first synapse in the visual system. It forms large-conductance homomeric channels that desensitize only modestly in response to ligand [10]. Many regions of the CNS are devoid of histaminergic neurons [11, 12], raising the possibility that Ort could be used to artificially inactivate specific neurons in these regions. To test this idea, we performed in vivo whole-cell recordings from antennal lobe neurons misexpressing Ort. In these neurons, histamine produced a rapid and reversible drop in input resistance, clamping the membrane potential below spike threshold and virtually abolishing spontaneous and odor-evoked activity. Every neuron type in this brain region could be inactivated in this manner. Neurons that did not misexpress Ort showed negligible responses to histamine. Ort also performed favorably in comparison to the available alternative effector transgenes. Thus, Ort misexpression is a useful tool for probing functional connectivity among Drosophila neurons.

    View details for DOI 10.1016/j.cub.2013.05.016

    View details for Web of Science ID 000321605600021

    View details for PubMedID 23770187

    View details for PubMedCentralID PMC3725270

  • Glutamate is an inhibitory neurotransmitter in the Drosophila olfactory system PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Liu, W. W., Wilson, R. I. 2013; 110 (25): 10294-10299

    Abstract

    Glutamatergic neurons are abundant in the Drosophila central nervous system, but their physiological effects are largely unknown. In this study, we investigated the effects of glutamate in the Drosophila antennal lobe, the first relay in the olfactory system and a model circuit for understanding olfactory processing. In the antennal lobe, one-third of local neurons are glutamatergic. Using in vivo whole-cell patch clamp recordings, we found that many glutamatergic local neurons are broadly tuned to odors. Iontophoresed glutamate hyperpolarizes all major cell types in the antennal lobe, and this effect is blocked by picrotoxin or by transgenic RNAi-mediated knockdown of the GluClα gene, which encodes a glutamate-gated chloride channel. Moreover, antennal lobe neurons are inhibited by selective activation of glutamatergic local neurons using a nonnative genetically encoded cation channel. Finally, transgenic knockdown of GluClα in principal neurons disinhibits the odor responses of these neurons. Thus, glutamate acts as an inhibitory neurotransmitter in the antennal lobe, broadly similar to the role of GABA in this circuit. However, because glutamate release is concentrated between glomeruli, whereas GABA release is concentrated within glomeruli, these neurotransmitters may act on different spatial and temporal scales. Thus, the existence of two parallel inhibitory transmitter systems may increase the range and flexibility of synaptic inhibition.

    View details for DOI 10.1073/pnas.1220560110

    View details for Web of Science ID 000321500200061

    View details for PubMedID 23729809

    View details for PubMedCentralID PMC3690841

  • Organic-inorganic interfaces and spiral growth in nacre JOURNAL OF THE ROYAL SOCIETY INTERFACE Yao, N., Epstein, A. K., Liu, W. W., Sauer, F., Yang, N. 2009; 6 (33): 367-376

    Abstract

    Nacre, the crown jewel of natural materials, has been extensively studied owing to its remarkable physical properties for over 160 years. Yet, the precise structural features governing its extraordinary strength and its growth mechanism remain elusive. In this paper, we present a series of observations pertaining to the red abalone (Haliotis rufescens) shell's organic-inorganic interface, organic interlayer morphology and properties, large-area crystal domain orientations and nacre growth. In particular, we describe unique lateral nano-growths and paired screw dislocations in the aragonite layers, and demonstrate that the organic material sandwiched between aragonite platelets consists of multiple organic layers of varying nano-mechanical resilience. Based on these novel observations and analysis, we propose a spiral growth model that accounts for both [001] vertical propagation via helices that surround numerous screw dislocation cores and simultaneous 010 lateral growth of aragonite sheet structure. These new findings may aid in creating novel organic-inorganic micro/nano composites through synthetic or biomineralization pathways.

    View details for DOI 10.1098/rsif.2008.0316

    View details for Web of Science ID 000264357800004

    View details for PubMedID 18753125

    View details for PubMedCentralID PMC2572677

  • A Microfluidic Chamber for Analysis of Neuron-to-Cell Spread and Axonal Transport of an Alpha-Herpesvirus PLOS ONE Liu, W. W., Goodhouse, J., Jeon, N., Enquist, L. W. 2008; 3 (6): e2382

    Abstract

    Alpha-herpesviruses, including herpes simplex virus and pseudorabies virus (PRV), infect the peripheral nervous system (PNS) of their hosts. Here, we describe an in vitro method for studying neuron-to-cell spread of infection as well as viral transport in axons. The method centers on a novel microfluidic chamber system that directs growth of axons into a fluidically isolated environment. The system uses substantially smaller amounts of virus inoculum and media than previous chamber systems and yet offers the flexibility of applying multiple virology and cell biology assays including live-cell optical imaging. Using PRV infection of cultured PNS neurons, we demonstrate that the microfluidic chamber recapitulates all known facets of neuron-to-cell spread demonstrated in animals and other compartmented cell systems.

    View details for DOI 10.1371/journal.pone.0002382

    View details for Web of Science ID 000263280700003

    View details for PubMedID 18560518

    View details for PubMedCentralID PMC2426917