SAIMSARA Journal

Machine Generated Science • ISSN 3054-3991

Pathophysiology of Deep Venous Thrombosis: Scoping Review with ☸️SAIMSARA.

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Vascular Health

Issue 1, Volume 1, 2026

Editorial note
• Last update: 2026-03-25 13:46:29
What is this paper about
This review shows that DVT is not just a problem of stasis — it is a biologically active inflammatory process driven by endothelial injury, platelet–leukocyte crosstalk, and NET-mediated immunothrombosis. Read the full paper to see which mechanisms are strongest, which patient phenotypes carry the clearest signals, and which emerging biomarkers and targets could reshape risk stratification and therapy.

DOI: 10.62487/saimsara66525623

Abstract: This paper aims to synthesize the current understanding of the pathophysiology of deep venous thrombosis by systematically extracting and integrating findings from recent research, thereby identifying key mechanistic pathways and potential areas for future investigation. The review utilises 96 studies. Across the mapped evidence, inflammatory activation and endothelial dysfunction repeatedly co-localize with platelet–leukocyte crosstalk and NET-associated immunothrombosis as prominent signals in DVT initiation and persistence. Clinically relevant gradients in risk were evident in specific inflammatory phenotypes, including increased VTE risk in inflammatory bowel disease (HR 2.12) and atopic dermatitis (HR 1.26), supporting the view that systemic inflammation can meaningfully shift thrombotic propensity beyond classic stasis-based explanations. Mechanistic submaps further indicate context-specific pathways—such as NF-κB–linked inflammation in cancer-associated DVT and hypoxia-responsive transcriptional programs at high altitude—highlighting that “DVT” likely comprises multiple overlapping endotypes with distinct triggers and potentially distinct biomarkers and targets. Practical implications include heightened vigilance and biomarker-informed risk stratification in high-risk settings (e.g., malignancy and inflammatory disease) and consideration of anatomical compression when presentations are atypical or recurrent. Future research should prioritize prospective human validation of leading immunothrombotic targets (e.g., platelet-derived HMGB1, Ral GTPases, CD39) and harmonized, cross-model studies that link thrombus composition and endothelial state to clinical outcomes such as post-thrombotic syndrome.

Keywords: Deep Venous Thrombosis; Pathophysiology; Neutrophil Extracellular Traps; Platelet Activation; Endothelial Dysfunction; Inflammation; Coagulation; Animal Models; Cancer-Associated Thrombosis; Postthrombotic Syndrome

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