Abstract
Purpose: This study aims to determine vitamin D concentrations in the vitreous and serum, as well as the expression levels of NLRP3 inflammasome pathway in the vitreous of patients with proliferative diabetic retinopathy (PDR). In addition, we investigated the possible correlation between NLRP3 inflammasome levels and vitamin D concentrations.Methods: We obtained vitreous samples before vitrectomy from 55 PDR patients, 25 non-diabetic patients with idiopathic macular hole (IMH), and 10 non-proliferative diabetic retinopathy (NPDR) patients. We also collected serum samples from the same patients. Enzyme-linked immunosorbent assay (ELISA) was used to examine NLRP3 inflammasome pathway proteins, including NLRP3, caspase-1, IL-1β, and VEGF. In addition, vitamin D concentrations were analyzed in Roche Cobas 6000's module e601 platform using electrochemiluminescence immune assay.Results: The levels of NLRP3 inflammasome pathway and VEGF increased dramatically in PDR vitreous. However, vitamin D concentrations in vitreous and serum followed the opposite trend. Meanwhile, vitreous and serum vitamin D concentrations were significantly negatively correlated with vitreous NLRP3 expression in PDR patients. Moreover, serum and vitreous vitamin D concentrations were positively correlated and demonstrated discriminatory ability in DR. The subgroup analysis of PDR group revealed that eyes with tractional retinal detachment (TRD) had higher NLRP3 inflammasome pathway and VEGF levels but lower vitamin D concentrations. Conversely, eyes that received preoperative pan-retinal photocoagulation (PRP) exhibited lower levels of NLRP3 inflammasome pathway, but vitamin D concentrations were irrelevant to laser treatment.Conclusions: Our results demonstrate a strong correlation between increased NLRP3 inflammasome pathway and decreased vitamin D concentrations in the vitreous of PDR patients, which may be linked to PDR pathogenesis. In addition, vitamin D supplementation may play a key role in preventing, treating, and improving PDR prognosis due to its inhibitory impact on NLRP3 inflammasome pathway and VEGF.
Highlights
Diabetic retinopathy (DR) is the most frequent microvascular complication of diabetes, causing blindness and vision impairment in the working-age population worldwide [1]
Our research group and Chaurasia et al demonstrated that reactive oxygen species (ROS)/TXNIP/NLRP3 inflammasome pathway is a major mechanism in DR and that NLRP3 inflammasome is involved in vascular impairment in the advanced stages of the disease [6, 7]
Loukovaara et al discovered that caspase-1 and IL-18 levels were significantly higher in the vitreous of PDR eyes than nonproliferative diabetic retinopathy (NPDR) eyes [12], confirming the dominating role of NLRP3 in PDR pathogenesis
Summary
Diabetic retinopathy (DR) is the most frequent microvascular complication of diabetes, causing blindness and vision impairment in the working-age population worldwide [1]. About 35% of diabetes patients suffer from DR, 6.8% have diabetic macular edema, 7.0% have proliferative diabetic retinopathy (PDR), and 10.2% have vision-threatening DR [2]. Numerous sophisticated treatments, including anti-vascular endothelial growth factor (VEGF) therapy and vitrectomy, can minimize the vision loss of severe DR patients. DR pathogenesis, proliferative diabetic retinopathy (PDR), remains unclear. Our research group and Chaurasia et al demonstrated that ROS/TXNIP/NLRP3 inflammasome pathway is a major mechanism in DR and that NLRP3 inflammasome is involved in vascular impairment in the advanced stages of the disease [6, 7]. Loukovaara et al discovered that caspase-1 and IL-18 levels were significantly higher in the vitreous of PDR eyes than nonproliferative diabetic retinopathy (NPDR) eyes [12], confirming the dominating role of NLRP3 in PDR pathogenesis
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