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Background: Diabetic retinopathy (DR) is the leading cause of blindness among the working-age population. The earliest morphological manifestation of the disease is pericyte loss, as shown by animal models.
Aims: The purpose of this study was to evaluate the presence of pericytes in vitreous samples (VS) from diabetic and nondiabetic patients.
Methods: VS from 125 patients with and without diabetes were analyzed. Thirty-three of the VS contained blood vessels and were therefore included in further analysis. Pericyte status was evaluated using α-smooth muscle actin and quantified using the following scoring system: total loss (3), >50% loss (2), <50% loss (1), and no loss (0).
Results: Of the 33 VS, 29 samples were from patients with diabetes and 4 from nondiabetic patients. Six diabetic cases had a score of 1, 8 diabetic cases had a score of 2, and 15 cases had a score of 3. A positive correlation between glycemia levels and pericyte loss was observed (p = 0.0016; Spearman's r = 0.61). Moreover, all nondiabetic cases had a score of 0 (sensitivity and specificity = 100%).
Conclusion: Pericyte loss in VS might be a sensitive and specific marker of DR that correlates with glycemia levels. Furthermore, VS, which are currently discarded, may contain valuable information for diabetic management.
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http://dx.doi.org/10.1159/000445212 | DOI Listing |
Biochim Biophys Acta Rev Cancer
August 2025
Department of Neurosurgery, Wuhan Union Hospital, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Glioma, the most prevalent primary malignant tumor of the central nervous system, exhibits aggressive progression and poor prognosis, largely due to its highly immunosuppressive tumor microenvironment (TME). Glioma-associated mesenchymal stem cells (GA-MSCs), a key component of the glioma TME, play a dual and context-dependent role in tumor biology. On one hand, GA-MSCs actively shape immunosuppression by interacting with various immune cells-including T cells, B cells, natural killer (NK) cells, dendritic cells (DCs), and macrophages-via soluble factors (e.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
August 2025
Cellular Signalling Laboratory, Department of Biochemical and Neuromotor Sciences, Alma Mater Studiorum, University of Bologna, Italy. Electronic address:
Collagen VI-related myopathies (COLVI-RMs) are rare genetic disorders caused by impaired assembly and secretion of COLVI, a key extracellular matrix (ECM) protein. COLVI deficiency alters ECM architecture and biomechanics, leading to progressive muscle fiber damage and connective tissue abnormalities. While pericytes are emerging as key players in muscle regeneration due to their myogenic potential, their role in COLVI-RMs remains unclear.
View Article and Find Full Text PDFPhytomedicine
September 2025
Department of Neurology, Zhongnan Hospital Affiliated to Wuhan University, Wuhan 430000, China. Electronic address:
Background: The leakage of vasa vasorum (VV) and intraplaque hemorrhage (IPH) pose significant risk for the instability and rupture of atherosclerosis (AS) plaques. The development of novel herbal monomers for anti-AS therapy has emerged as an increasingly promising strategy in combating cardiovascular diseases and stroke, which are frequently triggered by the rupture of vulnerable plaques.
Purpose: This study aimed to explore the protective effects of theaflavin-3,3'-digallate (TFDG) on plaque stability and its underlying mechanisms in preventing IPH through promoting VV maturation.
J Egypt Natl Canc Inst
June 2025
Instituto Nacional de Cancerología, Bogotá, Colombia.
Background: Pleural mesothelioma (PM) is an aggressive cancer with poor prognosis, often driven by asbestos exposure. Mutations in the NF2 gene, a key regulator of the Hippo signaling pathway, are frequently observed in PM. However, their impact on tumor biology, immune infiltration, cytokine signaling, and therapeutic response remains poorly understood.
View Article and Find Full Text PDFJ Neurochem
June 2025
Division of Medical Sciences, University of Victoria, Victoria, British Columbia, Canada.
Alzheimer's disease (AD) involves cognitive decline, possibly via multiple concurrent pathologies associated with iron accumulation. To investigate if iron accumulation in AD is more likely due to pathological iron-rich compartments, or a compensatory response of iron within oligodendrocytes to disease progression, we sought to quantify iron-rich staining (via Perl's diaminobenzidine; DAB). Healthy wild-type (WT) and APP-PS1Δe9 (APP-PS1; amyloid-beta overexpressing) male mice were examined during middle age, at 14 months.
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