Key result
Obesity and thrombophilia drive cardiovascular disease and thrombosis via proinflammatory and prothrombotic adipokines.
Why the study?
The pathogenetic mechanisms linking obesity, cardiovascular diseases, thrombosis, and thrombophilia are under active study to understand their roles in atherothrombotic risk.
This review highlights the pathogenetic mechanisms linking obesity, adipocyte-derived cytokines, and thrombophilia to increased atherothrombotic risk.
Answers are grounded in this paper and cite their sources.
Highlights mechanistic pathways without supporting practice change; leaves open targeted interventional trials in obese patients with thrombophilia.
The assosiation between obesity, cardiovascular diseases and thrombosis is well-known and is caused by proinflammatory and prothombotic status in obesity. Numerous hormones and cytokines, secreted by adipocytes, influence the gene expression and function of endothelial cells, arterial smooth muscle cells, and monocytes leading to the development of an atherosclerotic plaque. Also, variety of cytokines produced by adipocytes controls endothelial function, hemostatic and fibrinolytic systems, platelet function, affecting progression of thombus formation. Nowadays,pathogenetic mechanisms of this relationship are under active study. Thrombophilia is another independent risk factor of tromboembolic complications.
No takes yet. Share an insight, caveat, or question.
А. В. Хромылев (2015) conducted a review in Obesity, cardiovascular diseases, and thrombosis. Obesity and thrombophilia was evaluated. Obesity and thrombophilia are associated with cardiovascular diseases and thrombosis through proinflammatory and prothrombotic mechanisms involving adipocyte-secreted hormones and cytokines.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: