Low expression of RBP4 in the vitreous humour of patients with proliferative diabetic retinopathy who underwent Conbercept intravitreal injection

Li, Hui; An, Weiting; Hong, Yaru; Zhao, Qi; Cao, Jingjing; Zhang, Xiaomin; Li, Xiaorong; Jy, Han; Dong, Lijie

doi:10.1016/j.exer.2022.109197

Cited by 1 publication

(1 citation statement)

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“…In this study, we linked RBP4 and tip cell formation, the vanguard of angiogenesis, to investigate the specific mechanism of RBP4 in neovascularization. Interestingly, it has been reported that RBP4 levels were elevated in the vitreous of patients with PDR disease and decreased after administration of anti-VEGF therapy, further demonstrating the potential value of RBP4 in RNV [ 61 ]. However, more complex mechanisms involving metabolism, immunity, neovascularization and fibrosis may remain to be elucidated given the unique pathologic state of diabetes.…”

Section: Discussionmentioning

confidence: 99%

Succinate-induced macrophage polarization and RBP4 secretion promote vascular sprouting in ocular neovascularization

Shen,

Lin,

et al. 2023

J Neuroinflammation

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Pathological neovascularization is a pivotal biological process in wet age-related macular degeneration (AMD), retinopathy of prematurity (ROP) and proliferative diabetic retinopathy (PDR), in which macrophages (Mφs) play a key role. Tip cell specialization is critical in angiogenesis; however, its interconnection with the surrounding immune environment remains unclear. Succinate is an intermediate in the tricarboxylic acid (TCA) cycle and was significantly elevated in patients with wet AMD by metabolomics. Advanced experiments revealed that SUCNR1 expression in Mφ and M2 polarization was detected in abnormal vessels of choroidal neovascularization (CNV) and oxygen-induced retinopathy (OIR) models. Succinate-induced M2 polarization via SUCNR1, which facilitated vascular endothelial cell (EC) migration, invasion, and tubulation, thus promoting angiogenesis in pathological neovascularization. Furthermore, evidence indicated that succinate triggered the release of RBP4 from Mφs into the surroundings to regulate endothelial sprouting and pathological angiogenesis via VEGFR2, a marker of tip cell formation. In conclusion, our results suggest that succinate represents a novel class of vasculature-inducing factors that modulate Mφ polarization and the RBP4/VEGFR2 pathway to induce pathological angiogenic signaling through tip cell specialization. Graphical Abstract

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Section: Discussionmentioning

confidence: 99%