Dr. Apte has established himself as the leading clinician-scientist in the area of ocular inflammation, angiogenesis, and disease pathogenesis. His groundbreaking work on macrophage activation, polarization, and inflammation in blinding diseases such as macular degeneration have not only enhanced our understanding of age-associated eye disease, but have also provided critical insights into seemingly unrelated systemic diseases including atherosclerosis, where macrophage mediated inflammation is critical.

Seminal studies performed in Dr. Apte’s laboratory demonstrated that it was the innate compartment of the immune system that regulated pathogenic neovascularization. In age-related macular degeneration (AMD), he demonstrated that classically activated macrophages (M1) are inhibitory to the development of neovascularization and alternatively activated macrophages (M2) are stimulatory. These important findings may explain why the incidence of AMD increases substantially with age. A cardinal manifestation of early AMD in the eye is the development of lipid-rich deposits called drusen underneath the retina. Factors that determined progression to the advanced, blinding forms of the disease were unclear until recent studies from his laboratory demonstrated that the robust cholesterol efflux capacities of macrophages trafficking through the eye were critical in preventing the development of pathologic neovascularization in AMD.

Recent work in his laboratory has expanded to several areas that include (i) the role of non-coding RNA in regulating the aging of the immune system, (ii) the mechanisms by which autophagic flux in macrophages regulates inflammatory eye disease, and (iii) NAD biosynthesis and its influence on inflammation and photoreceptor survival.