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<p>Proliferative vitreoretinopathy (PVR) is the leading cause of failure after rhegmatogenous retinal detachment (RRD) repair, yet no baseline biomarkers exist to stratify risk. In this retrospective, nested case–control study we asked whether the vitreous proteome at the time of primary RRD repair predicts subsequent PVR. Undiluted vitreous (1.0 mL) was obtained by pars plana vitrectomy from 16 eyes of 16 patients (8 who later developed PVR and 8 matched RRD controls) and analyzed by tandem mass tag (TMT)-multiplexed liquid chromatography–tandem mass spectrometry. Of 918 proteins identified, 876 were retained after contaminant filtering. After Benjamini–Hochberg correction for multiple comparisons, no proteins were differentially expressed between cases and controls. Six proteins (decorin, arrestin-C, pre-mRNA processing factor 6, C-reactive protein, fructose-1,6-bisphosphatase 1 and an immunoglobulin kappa variable chain) reached nominal significance (<i>p</i> &lt; 0.05) but did not survive correction. The most abundant vitreous constituents included albumin, retinol-binding protein 4 and serotransferrin. In this limited cohort, no large or statistically robust baseline proteomic differences were detected between eyes that subsequently developed PVR and matched controls. We hypothesize that the molecular drivers of PVR may emerge postoperatively rather than being present at the time of the index detachment, although larger studies will be required to confirm or refute this possibility. Data are available via ProteomeXchange with identifier PXD077831.</p>

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The baseline vitreous proteome in rhegmatogenous retinal detachment: a case–control study of proliferative vitreoretinopathy

  • 期刊论文

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  • 发表日期：

    2026年7月10日

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  • Mary-Grace R. Reeves,
  • Matthew Yuan,
  • Sohini Rebba,
  • Philip A. Ruzycki,
  • P. Kumar Rao,
  • Rithwick Rajagopal

摘要

Proliferative vitreoretinopathy (PVR) is the leading cause of failure after rhegmatogenous retinal detachment (RRD) repair, yet no baseline biomarkers exist to stratify risk. In this retrospective, nested case–control study we asked whether the vitreous proteome at the time of primary RRD repair predicts subsequent PVR. Undiluted vitreous (1.0 mL) was obtained by pars plana vitrectomy from 16 eyes of 16 patients (8 who later developed PVR and 8 matched RRD controls) and analyzed by tandem mass tag (TMT)-multiplexed liquid chromatography–tandem mass spectrometry. Of 918 proteins identified, 876 were retained after contaminant filtering. After Benjamini–Hochberg correction for multiple comparisons, no proteins were differentially expressed between cases and controls. Six proteins (decorin, arrestin-C, pre-mRNA processing factor 6, C-reactive protein, fructose-1,6-bisphosphatase 1 and an immunoglobulin kappa variable chain) reached nominal significance (p < 0.05) but did not survive correction. The most abundant vitreous constituents included albumin, retinol-binding protein 4 and serotransferrin. In this limited cohort, no large or statistically robust baseline proteomic differences were detected between eyes that subsequently developed PVR and matched controls. We hypothesize that the molecular drivers of PVR may emerge postoperatively rather than being present at the time of the index detachment, although larger studies will be required to confirm or refute this possibility. Data are available via ProteomeXchange with identifier PXD077831.