Fig. 2

SRT and TSR presumed way of action. SRT (above) induces initial necrosis by photodisruption of RPE. Toll-like receptors (TLR) are expressed. Microglia (M) are attracted, interleukins (IL) and chemokines (CCL/CCX) are increased in expression thereby attracting more cells of the immune system. Destroyed cells are removed and neighboring RPE starts migration and proliferation to close the lesion. Increased matrix metallo-proteases (MMP) restructure Bruch’s membrane (BrM) and intra-BrM lipids (orange line) are removed. A rejuvenated, restored BrM/RPE complex is achieved thereafter. Neuroretina stays intact during this process. TSR (below) does not induce necrosis. It initially increases temperature within RPE leading to cell protective mechanisms, like the expression of heat shock proteins (HSP). Inflammatory processes, like interleukin expression and chemotaxis are initially suppressed. We hypothesize that single RPE cells die later and are instantly removed. This presumably apoptotic process, since cell death and replacement are seen in absence of inflammation, is accompanied by migration and proliferation of RPE cells. MMP expression is increased leading to BrM remodeling and removal of accumulated lipids (orange line). A rejuvenated restored BrM/RPE complex is achieved without damage to neuroretina. PR (photoreceptors), G (granulocytes), T (T-lymphocytes)