Philip Mzyk

Credentials: Department of Ophthalmology and Visual Sciences (School of Medicine and Public Health)

Position title: Postdoctoral Research Associate


3375 Medical Sciences Center
1300 University Ave
Madison, WI 53706

Advisor: Colleen McDowell, PhD

Keywords: Glaucoma, trabecular meshwork damage


BS 2012, Zoology, North Carolina State University, Raleigh, NC
PhD 2018, Comparative Biomedical Sciences, North Carolina State University, Raleigh, NC
Postdoctoral Fellow 2019, Glaucoma, Duke University, Durham, NC


Elevated IOP is one of the primary risk factors in the development of glaucoma. The trabecular meshwork (TM) is a critical tissue involved in the outflow of aqueous humor and regulation of IOP. Changes in the extracellular matrix (ECM) environment in the TM can alter the ability of aqueous humor to properly drain from the anterior chamber. The involvement of TGF-β2 signaling pathways in the regulation of the ECM in the TM has been extensively studied. Recent evidence has implicated toll-like receptor 4 (TLR4) in the regulation of ECM and fibrogenesis in other tissues such as liver, kidney, lung and skin. Dr. Mzyk and colleagues have discovered that a mutation in TLR4 rescues TGFβ2-induced ocular hypertension in mice. This discovery is a direct result of a careful mouse strain characterization utilizing the lab’s mouse model of TGFβ2-induced ocular hypertension. Based on these results, his work focuses on the hypothesis that crosstalk between TGFβ2 and TLR4 signaling leads to glaucomatous damage. These work could provide new targets to lower IOP and further explain the mechanisms involved in the development of glaucomatous TM damage.

McDowwell Lab