ArticleBMC ophthalmology2026
hsa_circ_0068631 facilitates the progression of diabetic retinopathy via regulating miR-140-5p in retinal microvascular endothelial cells.
Article in BMC ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiabetic retinopathy (DR), one of the most prevalent and clinically significant microvascular complications of diabetes mellitus, poses a significant challenge to public health worldwide. Circular RNAs (circRNAs) have emerged as critical regulators of the pathogenesis of various diseases.
aimTo investigate the role and underlying molecular mechanisms of circ_0068631 in the progression of DR.
methodsPlasma samples were collected from 80 patients with type 2 diabetes mellitus (T2DM) and 160 patients with DR, including 82 with non-proliferative DR (NPDR) and 78 with proliferative DR (PDR). circ_0068631 expression was measured by RT-qPCR, and its risk-predicitve potential for DR was evaluated using receiver operating characteristic (ROC) curves. In vitro experiments were performed using HG-treated human retinal microvascular endothelial cells (hRMECs) to assess cell function and the interaction between circ_0068631 and miR-140-5p. An enzyme-linked immunosorbent assay (ELISA) was utilized to measure the vascular endothelial growth factor (VEGF) concentration.
resultsPlasma circ_0068631 was upregulated in DR patients, especially in those with PDR, and displayed high risk-predictive value for distinguishing DR patients from T2DM (AUC = 0.913) and for identifying PDR among DR patients (AUC = 0.884). Silencing circ_0068631 inhibited viability, migration, and VEGF secretion in HG-treated hRMECs. circ_0068631 targeted miR-140-5p, and inhibiting miR-140-5p reversed the effects of circ_0068631 silencing.
conclusioncirc_0068631 promotes DR progression by targeting miR-140-5p in hRMECs, serving as a putative blood-based marker for assessing the severity of DR and a therapeutic target for treating DR.
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