Figure 1.

Proposed Model of the Potential Implications of Lysosomal Dysfunction in the Pathogenesis of POAG. The accumulation of lipofuscin-loaded lysosomes with diminished degradative capacity within aging TM cells might: (1) cause the accumulation of worn-out organelles and thus contribute to the progressive cellular dysfunction and tissue homeostasis associated with the aging process; (2) participate in collagen deposition due to inefficient intracellular and extracellular collagen degradation by lysosomal proteases; (3) impair the phagocytic TM cellular capacity and promote the accumulation of cellular debris and components of the ECM, in particular, collagen; and (4) induce lysosomal permeabilization with consequent TM cell death, which could explain the decreased cellularity, as well as the presence of extracellular lysosomal-related organelles in the glaucomatous TM.