ReviewFrontiers in immunology2025
Endothelial activation in thromboangiitis obliterans: mechanisms and therapeutic horizons.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Rheumatoid Factor Beyond Rheumatoid Arthritis: A Potential Marker of Cardiometabolic and Hepatic Risk.Biologics : targets & therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thromboangiitis obliterans (TAO) is a non-atherosclerotic, inflammatory vasculopathy characterized by thrombotic occlusion of small- and medium-sized vessels, leading to tissue ischemia and gangrene. Emerging evidence underscores endothelial cell (EC) activation as a central driver of disease progression, mediated by immune dysregulation, oxidative stress (Nrf2/ROS imbalance), impaired nitric oxide signaling (eNOS/iNOS dysregulation), endoplasmic reticulum and mitochondrial dysfunction, and disrupted copper/iron homeostasis. These pathways collectively promote a prothrombotic, proinflammatory endothelial phenotype, perpetuating vascular injury. Current therapies primarily alleviate symptoms but fail to address underlying EC dysfunction. Recent advances, including stem cell therapy and targeted immunomodulation, offer promising avenues for restoring endothelial homeostasis. However, translating mechanistic insights into durable clinical benefits requires further research into precision medicine approaches and large-scale validation of novel therapeutics. This review summarizes the multifactorial pathogenesis of TAO, emphasizing EC activation as a therapeutic linchpin, and outlines future directions to bridge translational gaps in disease management.
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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 Socratic graph.