New insights into the role of adipose tissue in thrombosis
Abstract
Central obesity is independently associated with an elevated risk of cardiovascular disease, particularly thrombotic complications. Increasing data supports a link between excess body weight and the risk to suffer acute myocardial infarction, stent thrombosis after percutaneous interventions, ischemic stroke and vein thrombosis. Experimental and in vitro data have provided insights as to the mechanisms currently presumed to increase the thrombotic risk in obese subjects. Obesity is characterized by a chronic low grade inflammation and systemic oxidative stress that eventually damage the endothelium losing its antithrombotic properties. Obesity also stimulates the expression of leptin and attenuates adiponectin release, a protective adipokine. Although the contribution of adipokines to thrombosis has been questioned, recent work has suggested that they enhance platelet activation and, although to a lesser extent, induce the coagulation cascade through tissue factor (TF) expression. Increased body weight also impairs platelet sensitivity to insulin signaling and enhances the production of bioactive isoprostanes further promoting platelet reactivity. Finally, obese subjects have shown elevated circulating levels of von Willebrand factor, TF, factor VII and VIII, and fibrinogen, favoring a mild-to-moderate hypercoagulable state, and, on the other hand, increased secretion of plasminogen activator inhibitor (PAI)-1 and thrombin activatable fibrinolysis inhibitor (TAFI) contributing to impair the fibrinolytic system. In the present review, we provide an overview of the impact of excess body weight on thrombosis. We will focus on the link between dysfunctional adipose tissue and endothelial damage, platelet reactivity, enhanced coagulation and impaired fibrinolysis; mechanisms currently recognized to increase arterial thrombotic risk in obese subjects.
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Additional evidence confirms that obesity is a contributing factor for type 2 diabetes, hypertension, and thrombotic episodes, as well as conditions linked to inflammation such as heart failure with preserved ejection fraction.
“Additional evi dence confirms that obesity is a contributing factor for type 2 diabetes, hypertension, and thrombotic ep isodes, as well as conditions linked to inflammation such as heart failure with preserved ejection frac tion. 2-7”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [2]
GGT reflects liver adiposity in addition to alcohol intake signals.
“liver adiposity in addi tion to alcohol intake signals (GGT)”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [2]
Leptin reflects total obesity or percent fat mass.
“consistent with their roles as biomarkers reflecting total obesity or percent fat mass (leptin)”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [2]
HOMA-IR reflects insulin resistance and ectopic and total fat.
“insulin resistance and ectopic and total fat (HOMA-IR). 2,29-31”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [2]
Increased platelet activity and thrombocytosis have been associated with obesity, particularly in women.
“Although increased platelet activity and thrombocytosis have been associated with obesity, particularly in women, 2,22”
From Comprehensive Long-Term Changes in Cardiovascular Risk Biomarkers With Tirzepatide (2026) · cites this paper as [2]
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- Authors
- Vilahur, G., Ben-Aicha, S., & Badimon, L.
- Affiliations
- Instituto de Salud Carlos III (ES)
- Corresponding author
- Vilahur, Gemma
- ORCID
- Vilahur, Gemma
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-05-03
- Volume
- 113
- Issue
- 9
- Pages
- 1046-1054
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- OpenAlex
- W2611087294
- Cited by
- 216
- References
- 98
- Citations by year
- 2026: 27 · 2025: 20 · 2024: 24 · 2023: 14 · 2022: 29 · 2021: 33 · 2020: 34 · 2019: 21 · 2018: 11 · 2017: 3
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Sociedad Española de Cardiología
- Ministerio de Ciencia e Innovación (SAF2016-76819-R, PNS 2015-71653-R, SAF2016-76819, PNS SAF2016-76819-R, 2015-71653)
- Centro de Investigación Biomédica en Red Enfermedades Cardiovasculares (CB16/11/00411)
- Instituto de Salud Carlos III ([CB16/11/00411], RD16/0011/018)
- Topics
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- obesity, thrombosis, adipose tissue dysfunction, abdominal obesity, endothelial dysfunction, platelet activation, isoprostanes, leptin, adiponectin, tissue factor, hypercoagulability, fibrinolysis, von Willebrand factor, plasminogen activator inhibitor-1, thrombin-activatable fibrinolysis inhibitor, acute myocardial infarction, ischemic stroke, venous thrombosis, stent thrombosis, oxidative stress, chronic inflammation
- MeSH terms
- Adipose Tissue, Animals, Blood Coagulation, Blood Coagulation Factors, Blood Platelets, Endothelium, Vascular, Humans, Risk Factors, Thrombosis, Signal Transduction, Adiposity, Adipokines, Obesity, Abdominal
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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