Retinal detachment is a serious ocular disease leading to photoreceptor degeneration and vision loss. However, the mechanism of photoreceptor degeneration remains unclear. The aim of this study was to investigate the altered metabolism pathway and physiological changes after retinal detachment. Eight-week-old male SD rats were fed, and the model of retinal detachment was established by injecting hyaluronic acid into the retinal space. The rats were euthanized 3 days after RD, and the retinal tissues were sectioned for analysis. Untargeted lipid chromatography-mass spectrometry lipidomic was performed to analyze the metabolite changes. A total of 90 significant metabolites (34 in anionic and 56 in cationic models) were detected after retinal detachment. The main pathways were (1) histidine metabolism; (2) phenylalanine, tyrosine, and tryptophan biosynthesis; and (3) glycine, serine, and threonine metabolism. The key genes corresponding to each metabolic pathway were verified from the Gene Expression Omnibus (GEO) database of human retinal samples. The results indicated that the production of histamine by histidine decarboxylase from histidine reduced after RD (p < 0.05). Xanthine, hypoxanthine, guanine, and guanosine decreased after RD (p < 0.05). Decreased xanthine and hypoxanthine may reduce the antioxidant ability. The decreased guanosine could not provide enough sources for inosine monophosphate production. Tyrosine is an important neurotransmitter and was significantly reduced after RD (p < 0.05). Citrate was significantly reduced with the increase of ATP-citrate lyase enzyme (ACLY) (p < 0.05). We inferred that lipid oxidation might increase rather than lipid biogenesis. Thus, this study highlighted the main changes of metabolite and physiological process after RD. The results may provide important information for photoreceptor degeneration.

The pathogenesis of myopia has been found to be associated with the blood supply of the choroid. This study aimed to determine the relationship between the distribution pattern of choroidal remodeling and the degree of myopia in young patients. Young patients (age < 18 years) with the spherical equivalent of less than − 12 diopters (D) were included. Spectral-domain optical coherence tomography (SD-OCT) with enhanced depth imaging (EDI) modality was used to measure the choroidal thickness (CT) and choroidal vascularity index (CVI) in the macular regions. CVI was calculated as the proportion of luminal area to choroidal area and was measured within 1 mm and 3 mm nasal (N1 and N3), temporal (T1 and T3), superior (S1 and S3), and inferior (I1 and I3) to the foveal center. CVI was compared across different ages (i.e., 5 ~ 9 years, 10 ~ 13 years, and 14 ~ 18 years), axial lengths (ALs) (i.e., 21.00 ~ 25.00 mm and 25.01 ~ 29.00 mm), and spherical equivalents (SEs) (i.e., SE > -0.5D, − 0.5 ~ − 3.0D, − 3.01 ~ − 6.0D, and < − 6.0D). Linear regression analysis was applied to assess the association between independent (i.e., age, AL, SE, and intraocular pressure) and dependent variables (i.e., CVI of different regions). One hundred sixty-four eyes from 85 volunteers were included. The mean CT in the central foveal was 269.87 ± 63.32 μm (93.00 μm to 443.00 μm). The mean subfoveal-CVI was 67.66 ± 2.40% (57.84 to 79.60%). Multiple linear regression results revealed significant correlations between SE and T1-CVI (p < 0.05, r² = 0.082, β = 0.194), N1-CVI (p < 0.05, r² = 0.039, β = 0.212). Simple linear regression results revealed that T1-CVI (p < 0.05, r² = 0.09) and T3-CVI (p < 0.05, r² = 0.05) were negatively correlated with SE; N1-CVI (p < 0.05, r² = 0.05) and N3-CVI (p < 0.05, r² = 0.04) were negatively correlated with SE. CVI in the horizontal meridian underwent the largest change as myopia worsened. Temporal and nasal CVIs within the r = 1 mm, and r = 3 mm subfoveal range were positively associated with the degree of myopia in young patients. The CVI value may be used to assess the vascular status of the choroid and be a potential marker of myopic progression.

Photoreceptor degeneration is a leading cause of visual impairment worldwide. Separation of neurosensory retina from the underlying retinal pigment epithelium is a prominent feature preceding photoreceptor degeneration in a variety of retinal diseases. Although ophthalmic surgeries have been well developed to restore retinal structures, post-op patients usually experience progressive photoreceptor degeneration and irreversible vision loss that is incurable at present. Previous studies point to a critical role of mitochondria-mediated apoptotic pathway in photoreceptor degeneration, but the upstream triggers remain largely unexplored. In this study, we show that after experimental RD induction, photoreceptors activate dynamin-related protein 1 (Drp1)-dependent mitochondrial fission pathway and subsequent apoptotic cascades. Mechanistically, endogenous ROS is necessary for Drp1 activation in vivo and exogenous ROS insult is sufficient to activate Drp1-dependent mitochondrial fission in cultured photoreceptors. Accordingly, inhibition of Drp1 activity effectively preserves mitochondrial integrity and rescues photoreceptors. Collectively, our data delineates a ROS-Drp1-mitochondria axis that promotes photoreceptor degeneration in retinal diseased models.