The long-term goal in Liton’s lab is to understand the molecular mechanisms underlying the normal physiology and the pathophysiology of the trabecular meshwork (TM)/Schlemms’s canal (SC) outflow pathway. The TM/SC is a complex tissue located in the anterior segment of the eye responsible of maintaining proper levels of intraocular pressure (IOP). Failure of this tissue function is associated with increase risk in developing Primary Open Angle Glaucoma (POAG), a potentially permanent blinding disease, affecting more than 70 million people worldwide.
Current efforts in our laboratory are focused on investigating a potential relationship between impairment of the autophagic lysosomal pathway and POAG. The lysosomal compartment is the cellular “garbage” disposal system responsible for the degradation of long-lived proteins and "worn out" organelles. We previously reported in the TM from glaucoma donors an increase in the number of cells with abnormal b-galactosidase activity at pH 6 (SA-b-Gal). More recent work showed that chronic exposure of TM cells to oxidative stress, a condition to which TM cells are known to be exposed in vivo during the aging process, causes the accumulation of nondegradable material within the lysosomal compartment leading to diminished lysosomal activity and increased expression of SA-b-Gal. Because the lysosomal compartment is responsible for maintaining general cellular turnover, we hypothesize such impaired activity may lead to a progressive cellular decline in the TM cell function, including TM phagocytic function, and thus contribute to the progression of POAG.
Education and Training
- Universidad Autonoma de Madrid (Spain), M.Sc. 1995
- Universidad Autonoma de Madrid (Spain), Ph.D. 2001