ArticleBlood advances2021
A targeted proteomics investigation of the obesity paradox in venous thromboembolism.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Proteomic Biomarkers in VTE: From Discovery to Clinical Translation.Journal of clinical medicine · 2026Review
- Adherence to the EAT-Lancet Diet, plasma proteomics, and risk of venous thromboembolism: a large-scale prospective cohort study.BMC medicine · 2026Article
- Proteomic Insights into Venous Thromboembolism.Medical sciences (Basel, Switzerland) · 2026Review
- The Interplay Between Obesity and Venous Thromboembolism: From Molecular Aspects to Clinical Issue.International journal of molecular sciences · 2025Review
- Biomarkers of Metabolism and Inflammation in Individuals with Obesity and Normal Weight: A Comparative Analysis Exploring Sex Differences.International journal of molecular sciences · 2025Article
- Obesity influences the biological response to injury: a multi-omics analysis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Persistent serum protein signatures define an inflammatory subcategory of long COVID.Nature communications · 2023Article
- Proteomics in thrombosis research.Research and practice in thrombosis and haemostasis · 2022Article
- Reassessing the Risk of Venous Thromboembolism (VTE) Events in Women.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisReview
- The epidemiology of early deep vein thrombosis in kidney transplant recipients.Canadian journal of surgery. Journal canadien de chirurgieObservational
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obesity paradox, the controversial finding that obesity promotes disease development but protects against sequelae in patients, has been observed in venous thromboembolism (VTE). The aim of this investigation was to identify a body mass-related proteomic signature in VTE patients and to evaluate whether this signature mediates the obesity paradox in VTE patients. Data from the Genotyping and Molecular Phenotyping in Venous ThromboEmbolism Project, a prospective cohort study of 693 VTE patients, were analyzed. A combined end point of recurrent VTE or all-cause death was used. Relative quantification of 444 proteins was performed using high-throughput targeted proteomics technology. Measurements were performed in samples collected during the acute VTE event and at 12-month follow-up. An 11-protein signature (CLEC4C, FABP4, FLT3LG, IL-17C, LEP, LYVE1, MASP1, ST2, THBS2, THBS4, TSLP) for body mass in VTE patients was identified. The signature did not significantly mediate the obesity paradox (change in hazard ratio [HR]: 0.04; likelihood ratio test of nested models = 7.7; P = .74), but its main constituent protein, leptin, was inversely associated with recurrent VTE or death (adjusted HR [95% confidence interval] per standard deviation increase: 0.66 [0.46-0.94]). This relationship was significantly (P = .007) modified by markers of leptin resistance (ie, high body mass index and high circulating matrix metalloproteinase-2 levels). Although the signature did not substantially explain the obesity paradox, leptin appears to be protective against disease recurrence and death in VTE patients. This protective effect was abrogated under conditions of leptin resistance and hence was unrelated to the obesity paradox.
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