Age-related macular degeneration (AMD) is a multifactorial disease, which can culminate in irreversible vision loss and blindness in elderly. Nowadays, there is a big gap between dry AMD and wet AMD on treatment. Accounting for nearly 90% of AMD, dry AMD still lacks effective treatment. Numerous genetic and molecular researches have confirmed the significant role of the complement system in the pathogenesis of AMD, leading to a deeper exploration of complement inhibitors in the treatment of AMD. To date, at least 14 different complement inhibitors have been or are being explored in AMD in almost 40 clinical trials. While most complement inhibitors fail to treat AMD successfully, two of them are effective in inhibiting the rate of GA progression in phase II clinical trials, and both of them successfully entered phase III trials. Furthermore, recently emerging complement gene therapy and combination therapy also offer new opportunities to treat AMD in the future. In this review, we aim to introduce genetic and molecular associations between the complement system and AMD, provide the updated progress in complement inhibitors in AMD on clinical trials, and discuss the challenges and prospects of complement therapeutic strategies in AMD.

Foot ulcers are a common complication of diabetes mellitus, which is associated with high morbidity and mortality among diabetic patients. The present study aims to investigate novel wound healing pathways in diabetic foot ulcers (DFU) through proteomics and a network pharmacology analysis. Tandem mass tag (TMT) labeled quantitative proteomics method was performed to evaluate the protein expression profile in wound tissues from healthy controls (HC) and DFU. Kyoto Encyclopedia of Genes (KEGG) and Genomes enrichment analysis (GO) was conducted based on differentially expressed proteins (DEPs) to discover the potential pathways associated with DFU. Western blot analysis was used to confirm the probable DFU-related targets. Proteomics analysis discovered 509 DEPs (248 upregulated and 261 downregulated proteins). Go and KEGG further evaluated the DEPs to discover the DFU-related pathways. According to network pharmacology study, three main targets (metalloproteinase 9 (MMP9), Fatty acid-binding protein 5 (FABP5), and integrin subunit alpha M (ITGAM)) play crucial roles in signaling pathways. Staphylococcus aureus infection and leukocyte transendothelial migration pathways significantly enriched in DFU. In addition, it was confirmed that three critical targets were elevated in diabetes mouse wound tissues. The study confirmed the presence of protein alterations in the wound-healing process of DFU mice and may provide fresh insights into the molecular mechanisms driving DFU.

Background: To investigate the structural and functional changes of the retina in patients with different degrees of internal carotid artery (ICA) stenosis. Methods: This cross-sectional study included patients with varying degrees ICA stenosis. Clinical characteristics of 41 patients were collected after being divided into four groups according to the ICA stenosis indicated by computed tomographic angiography (Group 0: without ICA stenosis, Group 1: ipsilateral slight ICA stenosis, Group 2: ipsilateral moderate ICA stenosis, Group 3: ipsilateral severe ICA stenosis). Retinal vessel caliber (RVC) was measured quantitatively with the Integrative Vessel Analysis software. The retinal sensitivity was examined with the MP-3 microperimeter. The relationships among central retinal artery equivalent (CRAE), central retinal vein equivalent, arteriole to venule ratio (AVR), mean retinal sensitivity (MS) and ICA stenosis degree were analysed. Results: The CRAE in Group 3 were significantly smaller compared with Group 0, Group 1 and Group 2 (P < 0.001, P < 0.001, P = 0.002). Significant decrease was found between Group 3 with other groups in MS at fovea (P < 0.001, P < 0.001, P = 0.002). Moreover, there was a positive correlation found between MS and CRAE (Beta = 0.60, P < 0.001 at fovea; Beta = 0.64, P < 0.001 at 2 degree; Beta = 0.60, P < 0.001 at 4 degree; Beta = 0.55, P < 0.001 at 8 degree; Beta = 0.53, P < 0.001 at 12 degree). Conclusions: The present study revealed smaller CRAE and AVR in ipsilateral severe ICA stenosis patients. And the MS decreased in patients with severe ICA stenosis. In addition, MS had a positive correlation with CRAE.

Wang H, et al. Korean J Radiol. 2021 Jul;22(7):1142-1151. https://doi.org/10.3348/kjr.2020.0178

Purpose. The association between β-peripapillary atrophy and the retinal vasculature in nonpathological high myopia is unclear. The aim of this study is to investigate whether β-peripapillary atrophy contribute to the changes of the retinal vasculature using optical coherence tomography angiography. Methods. In a cross-sectional study, one hundred and thirty eyes with nonpathological high myopia were included. β-peripapillary atrophy was analysed using Image J software based on fundus photographs. A 3.0 × 3.0 mm² grid and a 4.5 × 4.5 mm² grid were used to scan parafoveal and peripapillary regions using optical coherence tomography angiography, respectively. Vessel density and fractal dimensions of the retina and foveal avascular zone were analysed and quantified using en face projection images. Correlations between the vascular density, foveal avascular zone, and β-peripapillary atrophy were determined. Results. Using multivariate analysis, β-peripapillary atrophy was negatively correlated with the vessel density in radial peripapillary capillaries (p=0.002) even after adjusting for other variables. This relationship was also confirmed in the macula (superficial retinal plexus: p<0.05; deep retinal plexus: p<0.05). The vessel densities in the nasal and inferior sectors were more strongly correlated with β-peripapillary atrophy. Conclusions. There was a negative correlation between β-peripapillary atrophy and the retinal vasculature in highly myopic eyes, especially in radial peripapillary capillaries and deep retinal plexus. β-peripapillary atrophy can be visualized and is a convenient structural feature that can benefit the early diagnosis and detection of chorioretinal atrophy in high myopia.