Effect of cytokine TGF-β1 on pathological changes in diabetic retinopathy

Abstract

The purpose of the study was to determine the role of the cytokine transforming growth factor beta 1 (TGF-β1) in the progression of diabetic retinopathy and to assess its importance as a potential therapeutic target for slowing down pathological changes in the retina. To achieve this goal, scientific publications selected from leading international databases were analysed. The studies investigated the molecular mechanisms of TGF-β1 activation, including Smad-dependent and Smad-independent pathways, such as MAPK, PI3K/Akt, Wnt/β-catenin and NF-κB, which play a key role in fibrotic, angiogenic and inflammatory processes. Particular attention was paid to the interaction of TGF-β1 with vascular endothelial growth factor (VEGF), which promotes the formation of new pathological vessels with increased permeability, as well as the regulation of the extracellular matrix. The analysis revealed that TGF-β1 is a key regulator of structural changes in the retina under hyperglycaemia, affecting basement membrane thickening, disruption of the blood-retinal barrier, increased vascular permeability and the development of chronic inflammation. It has been shown that elevated levels of TGF-β1 contribute to the progression of fibrosis by activating the epithelial-mesenchymal transition of retinal pigment epithelial cells, which leads to tissue remodelling. In addition, it was found that activation of TGF-β1 under the influence of hyperglycaemia is associated with increased oxidative stress, inflammatory reactions and angiogenesis. The analysis of experimental studies in animal models where streptozotocin was used to induce hyperglycaemia, as well as clinical observations of patients with diabetic retinopathy, allowed to assess the effectiveness of TGF-β1 inhibitors in reducing fibrotic changes, angiogenesis, and chronic inflammation. The results obtained contribute to the formation of a theoretical basis for the further development of therapeutic strategies aimed at inhibiting TGF-β1 as an important component of the pathogenesis of diabetic retinopathy.

Keywords: Hyperglycaemia; Inflammation; Molecular mechanisms; Retina; Signalling pathways.