ArticleCells2025
ADAMTS13 Improves Endothelial Function and Reduces Inflammation in Diabetic Retinopathy.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Bone marrow fibrocytes and endothelial-to-mesenchymal transition drive pathological ECM remodeling in proliferative diabetic retinopathy.Molecular and cellular biochemistry · 2026Article
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Evaluation of Endothelial Dysfunction in Geriatric Patients with Non-Dialysis Chronic Kidney Disease.Journal of clinical medicine · 2026Article
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Cold atmospheric plasma is a promising strategy for treating diabetic retinopathy.Journal of translational medicine · 2025Review
- Article
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- An Expendable Player in Positive Vascular Remodeling? ADAMTS13 Deficiency Does Not Affect Arteriogenesis or Angiogenesis.International journal of molecular sciences · 2025Article
- Perioperative Profiling of a Disintegrin and Metalloprotease with Thrombospondin Type 1 Motif, Member 13 (ADAMTS13) Activity in Cardiac Surgery: Kinetics and Mechanistic Insights.Journal of clinical medicine · 2025Article
- Decreased miR-455-3p promotes diabetic retinopathy progression via modulating retinal endothelial proliferation and apoptosis.BMC ophthalmology · 2025Article
- Aqueous humor levels of syndecan-1 and syndecan-4 associated with OCTA metrics in diabetic retinopathy.Frontiers in medicine · 2025Article
- RUNX1 promotes pathological retinal angiogenesis through von Willebrand factor.Advances in ophthalmology practice and researchArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
The protease, a disintegrin and metalloproteinase with thrombospondin type 1 motif member 13 (ADAMTS13), known to cleave only the von Willebrand factor (VWF), has powerful regulatory effects on microvascular platelet adhesion, thrombosis, inflammation, and endothelial dysfunction. We study the protection against diabetes-induced retinal injury in experimental rats by supplementation with recombinant ADAMTS13. We compare human epiretinal membranes and vitreous samples from nondiabetic subjects and patients with proliferative diabetic retinopathy (PDR) and extend in vitro analyses with the use of various immunodetection and spectrofluorimetric methods on rat retina and human retinal glial and endothelial cell cultures. Functional studies include the assessment of the blood-retinal barrier (BRB), cell adhesion, and in vitro angiogenesis. In epiretinal membranes, endothelial cells and monocytes/macrophages express ADAMTS13. The levels of VWF, the platelet marker CD41, ADAMTS13, and the biomarkers of endothelial cell injury soluble VE-cadherin and soluble syndecan-1 are increased in PDR vitreous. ADAMTS13 is downregulated in diabetic rat retinas. The intravitreal administration of ADAMTS13 attenuates diabetes-induced BRB breakdown, the downregulation of VE-cadherin and β-catenin, and the upregulation of VWF, CD41, phospho-ERK1/2, HMGB1, VCAM-1, and ICAM-1. In Müller cells, ADAMTS13 attenuates MCP-1, MMP-9, and ROS upregulation induced by diabetic mimetic conditions. In HRMECs, ADAMTS13 attenuates the shedding of the soluble VE-cadherin and soluble syndecan-1 and the levels of phospho-ERK1/2, MCP-1, fractalkine, and ROS induced by diabetic mimetic conditions, the upregulation of ICAM-1 and VCAM-1 elicited by TNF-α, the adherence of monocytes induced by TNF-α, and VEGF-induced migration of human retinal microvascular endothelial cells. Our findings suggest that enhancing ADAMTS13 levels in situ ameliorates diabetes-induced retinal inflammation and vascular dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.