The role of clusterin as an antiapoptotic glial factor in the development of diabetic machular edema in patients with type 2 diabetes mellitus

S.А. Suk, S.O. Rykov, M.L. Kyryliuk


Background. One of the important modern factors that plays an important role in restoring close contacts and limiting the reactive response to metabolic damage (two main signs of the pathogenesis of diabetic macular edema (DME)) is the clusterin protein. The research of its contribution into the development of DME has recently been actively started. We previously found that at the initial stages of DME and its progression, the blood level of clusterin was elevated above the threshold (77 μg/ml). Its level was associated with an increased risk of thickening of the nerve fibers layer and ganglio­nar layer. The study of clusterin expression and its relationship with these indicators at the different stages of DME development is rele­vant. The purpose of the work was to evaluate the role of clusterin as an antiapoptotic glial factor in the development of diabetic macular edema in patients with type 2 diabetes mellitus. Material and methods. The study involved 82 patients with DMT2 (145 eyes), divided into 4 groups in accordance with DME form. The average age of patients was 65.25 ± 10.85 years; the average duration of diabetes mellitus was 14.0 ± 7.05 years; the average level of HbA1c was 8.40 ± 1.58 %. Optical coherent tomography was performed using the Revo Nx Optopol spectral optical tomograph (5 μm axial resolution) using Retina 3D scanning protocol for macular thickness study. The following instrumental parameters were used for analysis: nerve fiber layer (NFL), ganglion cell layer (GCL) layer, internal posterior layer (IPL), central sector thickness, minimum foveal thickness, average thickness, macular volume and foveal volume, visual acuity. Results. Using ANOVA analysis and regression analysis, methods for constructing of logistic regression models, we have shown that clusterin is not associated with the risk of high value of NFL, GCL, IPL, central sector of macula, foveal thickness and low visual acuity in comparison with the initial stages of DME. Conclusions. We suggest the limited role of clusterin and its relative insufficiency in severe DME and the possibility for its use in situ as an additional therapeutic agent.


clusterin; diabetic macular edema; type 2 diabetes mellitus


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