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Retinal vein occlusion (RVO) and ischemic hypoxic retinopathy (IHR) are leading cause of irreversible vision loss worldwide, compelled by complex microvascular dysfunction, neuroinflammation, and tissue hypoxia. Despite advances in imaging and treatment, a comprehensive understanding of cellular and molecular heterogeneity underlying these pathologies remains limited. Recently, single-cell RNA sequencing (scRNA-seq) has emerged as a transformative technology, enabling unprecedented resolution of cellular dynamics, transcriptomic landscapes, and intracellular communication within the retina. Single-cell technologies continue to evolve, they are poised to revolutionize our understanding of retinal vascular diseases, ultimately paving the way for precision diagnostics and targeted interventions. This technique has revolutionized our understanding regarding complex biological systems and enables proper analysis of cellular heterogeneity. This review highlights the recent progress for the application SCS to dissect the pathophysiology of RVO and IHR. Moreover, current study summarizes findings on altered gene expression endothelial cells, Muller glia, micro glia and photoreceptors under ischemic and hypoxic stress, shedding light on potential therapeutic targets and biomarkers. Furthermore, this study explores the integration of snRNA-seq, spatial transcriptomics, and multi-omics approaches to enhance the spatial and temporal mapping of retinal responses. Additionally, discuss the current challenges, including sample preservation, retinal cell-type annotation, and cross-species translation, while offering insights into future directions such as personalized medicine and regenerative strategies. This paper aims to provide clinicians and researchers with a comprehensive update on the rapidly expanding frontier of single-cell analysis in retinal ischemic diseases.
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http://dx.doi.org/10.1016/j.exer.2025.110436 | DOI Listing |
Gene
September 2025
Institute of Physiology, Medical School, University of Pécs H-7624 Pécs, Hungary. Electronic address:
In this edition of Gene's "Editor's Corner" we summarize the complex interactions of different molecular mechanisms behind the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). The topic is relevant, as the therapeutic options for HIE are limited, it is important to have as much knowledge as possible about the molecular processes underlying the disease. In the recent issue of Gene (Gene 952, 2025, 149363), Wang et al.
View Article and Find Full Text PDFJ Neurophysiol
September 2025
Department of Radiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang 110004, China.
Neonatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of developmental disorders and permanent central nervous system damage, with functional recovery closely linked to myelin sheath integrity. This study aimed to analyze the expression of pH and the voltage-gated proton channel (Hv1) in the brains of neonatal pigs with HIE at various time points, alongside changes in myelin-related proteins. MRI was employed to localize the basal ganglia and assess pH changes post-hypoxia-ischemia, while immunofluorescence staining was used to evaluate Hv1, myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), and myelin-associated glycoprotein (MAG).
View Article and Find Full Text PDFPLoS One
September 2025
The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia, Baotou, China.
Background: Type 2 diabetes mellitus (T2DM) complicated with ischemic stroke is a major challenge to global public health and is related to poor prognosis. However, the role of blood urea nitrogen(BUN)to serum albumin ratio (BAR) in predicting in-hospital mortality of T2DM patients with ischemic stroke has not been fully explored. This study was carried out to investigate the relationship between BAR level and in-hospital mortality of T2DM patients with ischemic stroke.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiac Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.
View Article and Find Full Text PDFHerz
September 2025
Department of Cardiology, The Third Clinical College of Wenzhou Medical University, 326000, Wenzhou, Zhejiang, China.
Background: The protective function of the tetrandrine (TET)-mediated transient receptor potential vanilloid 2 (TRPV2) channel in myocardial ischemia/reperfusion injury (MI/RI) has been established in numerous investigations. The objective of the current study was to explain how TRPV2 further modulates downstream factors to influence the progression of MI/RI.
Methods: To this end, an MI/RI model in rats and a hypoxia-reoxygenation (H/R) cell model in H9c2 cells were constructed.