Beyond glycemia: The influence of systemic inflammation, lipids, and the gut-retina axis in diabetic retinopathy

Figure 4 The figure outlines the shift toward a multifactorial view of diabetic retinopathy, where inflammation, lipid imbalance, and gut dysbiosis interact to drive neurovascular dysfunction. These interconnected pathways link metabolic stress to retinal inflammation, barrier disruption, and neuronal injury, redefining diabetic retinopathy as a systemic immune-metabolic disease beyond hyperglycemia. NF-κB: Nuclear factor kappa B; IL: Interleukin; TNF-α: Tumor necrosis factor-alpha; NLRP3: NLR family pyrin domain-containing 3; SCFA: Short chain fatty acids; BRB: Blood-retinal barrier; LXR: Liver X receptors; ABCA1/ABCG1: ATP-binding cassette transporter A1/G1; sEH: Soluble epoxide hydrolase.