Diabetes mellitus (DM) is a complex metabolic syndrome characterized by hyperglycemia. Diabetic retinopathy (DR) is the most common complication of DM and the leading cause of blindness in the working-age population of the Western world. Lipopolysaccharides (LPS) is an essential ingredient of the outer membrane of gram-negative bacteria, which induces systemic inflammatory responses and cellular apoptotic changes in the host. High-level serum LPS has been found in diabetic patients at the advanced stages, which is mainly due to gut leakage and dysbiosis. In this light, increasing evidence points to a strong correlation between systemic LPS challenge and the progression of DR. Although the underlying molecular mechanisms have not been fully elucidated yet, LPS-related pathobiological events in the retina may contribute to the exacerbation of vasculopathy and neurodegeneration in DR. In this review, we focus on the involvement of LPS in the progression of DR, with emphasis on the blood-retina barrier dysfunction and dysregulated glial activation. Eventually, we summarize the recent advances in the therapeutic strategies for antagonising LPS activity, which may be introduced to DR treatment with promising clinical value.
Keywords: Blood-retina barrier; Diabetic retinopathy; Dysbiosis; Gut leakage; Inflammation; Lipopolysaccharides; Retinal glia.
© 2022. The Author(s).