The role of
inflammation in
diabetic retinopathy (DR) is well-established and dysregulation of a large number of inflammatory mediators is known. These include
cytokines,
chemokines,
growth factors, mediators of proteogenesis, and pro-apoptotic molecules. This para-
inflammation as a response is not directed to a particular pathogen or
antigen but is rather directed toward the by-products of the diabetic milieu. The inflammatory mediators take part in cascades that result in cellular level responses like neurodegeneration, pericyte loss, leakage, capillary drop out, neovascularization, etc. There are multiple overlaps between the inflammatory pathways occurring within the diabetic retina due to a large number of mediators, their varied sources, and cross-interactions. This makes understanding the role of
inflammation in clinical manifestations of DR difficult. Currently, mediator-based
therapy for DR is being evaluated for interventions that target a specific step of the inflammatory cascade. We reviewed the role of
inflammation in DR and derived a simplified clinicopathological correlation between the sources and stimuli of
inflammation, the inflammatory mediators and pathways, and the clinical manifestations of DR. By doing so, we deliberate mediator-specific
therapy for DR. The cross-interactions between inflammatory mediators and the molecular cycles influencing the inflammatory cascades are crucial challenges to such an approach. Future research should be directed to assess the feasibility of the pathology-based
therapy for DR.