Dr. Wang completed his medical education, including a Masters in Science degree, and worked as an ophthalmologist specializing in glaucoma in China. He earned his Ph.D. in ocular vascular physiology at Uppsala University, Sweden, mentored by Prof. Anders Bill. He carried out his postdoctoral training at Devers Eye Institute with Drs. Van Buskirk and Cioffi and participated in multiple research projects.
As an Associate Scientist at Legacy Research Institute, he has applied his expertise to investigate vascular pathology in experimental models of neurodegeneration and glaucoma. He is now focusing on the role of glial cells in vascular physiology and glaucoma by using a rodent experimental model combined with in vivo imaging techniques, molecular biology, and transgenetic methods. His studies have been continuously funded by the National Institutes of Health, the BrightFocus Foundation, the Glaucoma Research Foundation, and Legacy Good Samaritan Foundation.
Glial Cell Contribution to Basal Vessel Diameter and Pressure-Initiated Vascular Responses in Rat Retina.
Li H, Bui BV, Cull G, Wang F, Wang L.
Invest Ophthalmol Vis Sci. 2017 Jan 1;58(1):1-8.
Optic nerve head blood flow response to reduced ocular perfusion pressure by alteration of either the blood pressure or intraocular pressure.
Wang L, Cull GA, Fortune B.
Curr Eye Res 2015;40:359-367.
Compromised Optic Nerve Blood Flow and Autoregulation Secondary to Neural Degeneration.
Cull G, Told R, Burgoyne CF, Thompson S, Fortune B, Wang L.
Invest Ophthalmol Vis Sci. 2015 Nov;56(12):7286-92.
In many diseases, such as diabetes and glaucoma, ocular tissues can be damaged due to too much blood (over-perfusion) or too little blood (ischemia) coming into the eye. One theory that interprets underlying mechanism for the disrupted blood supply is the failure of the regulatory system which determines exactly how much blood enters the eye, also known as “autoregulation”. Dr. Wang’ research interests have been focused on how the regulatory system works, the relationship between dysfunctional autoregulation and optic nerve tissue damage, and what cell types are responsible during this process in normal and glaucomatous eyes.
By using an optic nerve ischemia model, he and his colleagues have demonstrated that inducing local ischemia around the optic nerve causes glaucomatous-like damage. It was further demonstrated that blood flow in the optic nerve surprisingly increases during the early stage before a progressive decline. The second surprising insight was that the autoregulation dysfunction within the optic nerve head manifests very differently to that seen in other tissues, and does not follow the general concept of autoregulation. These unique hemodynamic changes in autoregulation during diseased conditions lead to a new research direction.
In a project recently funded by the National Institutes of Health, Dr. Wang will be investigating the role of glial cells in blood flow autoregulation by using devices that are capable of simultaneously monitoring the vasculature and activities of glial cells while intravascular and extravascular pressures are instrumentally controlled.
The research conducted by Dr. Wang is expected to benefit glaucoma patients by helping us to better understand mechanisms of blood flow autoregulation, and the relationship between ocular microcirculation and glaucomatous optic nerve damage.