Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

The Interplay Between Obesity and Venous Thromboembolism: From Molecular Aspects to Clinical Issue

Zawadzka PS., Imiela AM., Pruszczyk P.

Narrative Review on Hip, published in Int J Mol Sci (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Int J Mol Sci (2025)
Reported sample size
—
Source database
Europe PMC
PMID
41226331
PMCID
PMC12610251
DOI
10.3390/ijms262110292
Citations
2

Abstract (original English)

This review examines the intricate relationship between obesity and venous thromboembolism (VTE), highlighting the underlying pathophysiological mechanisms and clinical implications. Obesity is an established independent risk factor for VTE, which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). The risk of VTE escalates with increasing body mass index (BMI) and is particularly associated with abdominal adiposity. Dysfunctional adipose tissue (AT) in obesity promotes a pro-thrombotic state through chronic low-grade inflammation and impaired fibrinolysis. This inflammation is driven by stress within hypertrophied adipocytes, which leads to localized hypoxia, cellular dysfunction, and ultimately, cell death. This inflammation is driven by adipocyte stress and the infiltration of immune cells. The adipokine leptin exemplifies the complex link between obesity and VTE. While leptin has pro-thrombotic effects, low leptin levels are paradoxically associated with an increased morbidity and mortality in patients with acute PE, a phenomenon termed the "obesity paradox". Furthermore, metabolic syndrome significantly increases the risk of recurrent VTE, with the risk growing with each additional metabolic component. Ultimately, a deeper understanding of the molecular and cellular links between obesity and VTE is essential for developing targeted strategies to reduce risk an

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Adipose TissueAnimalsHumansObesityInflammationLeptinRisk FactorsVenous Thromboembolism

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