Current opinion in hematology · 2026
Bidirectional relationship between metabolic and thrombotic disease mechanisms.
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Jameson Angelica T, Hur Woosuk S
Аннотация
PURPOSE OF REVIEW: Metabolic diseases, including obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), and diabetes, are associated with increased thrombotic risks. Conversely, components of the hemostatic system influence the development of metabolic pathologies, suggesting a bidirectional relationship between metabolic and thrombotic diseases. This review provides an update on recent advances in the mechanisms by which metabolic pathologies drive thrombosis and how hemostatic system components modulate metabolic diseases.
RECENT FINDINGS: Novel insights into fibrinolytic changes as a driver of thrombosis, improved thrombotic risk prediction models, synergistic thrombotic effect with other prothrombotic conditions in metabolic pathologies as well as the impact of weight loss therapies on metabolic dysfunction-associated thrombosis are discussed. Furthermore, recent updates on the roles of urokinase plasminogen activator and factor XIIIA (FXIIIA) in metabolic pathology development are highlighted.
SUMMARY: Metabolic pathologies suppress fibrinolytic activity and are largely driven by elevated plasminogen activator inhibitor 1 (PAI-1) levels. Development of novel strategies targeting PAI-1 to attenuate thrombotic risks are in progress. Weight loss following bariatric surgery is associated with reduced thrombotic risk, though the impact of glucagon-like peptide 1 receptor agonist on obesity-associated cardiovascular disease risk remains unclear. Conversely, new insights identify urokinase and FXIIIA as promoters of metabolic dysfunction, particularly MASLD.
RECENT FINDINGS: Novel insights into fibrinolytic changes as a driver of thrombosis, improved thrombotic risk prediction models, synergistic thrombotic effect with other prothrombotic conditions in metabolic pathologies as well as the impact of weight loss therapies on metabolic dysfunction-associated thrombosis are discussed. Furthermore, recent updates on the roles of urokinase plasminogen activator and factor XIIIA (FXIIIA) in metabolic pathology development are highlighted.
SUMMARY: Metabolic pathologies suppress fibrinolytic activity and are largely driven by elevated plasminogen activator inhibitor 1 (PAI-1) levels. Development of novel strategies targeting PAI-1 to attenuate thrombotic risks are in progress. Weight loss following bariatric surgery is associated with reduced thrombotic risk, though the impact of glucagon-like peptide 1 receptor agonist on obesity-associated cardiovascular disease risk remains unclear. Conversely, new insights identify urokinase and FXIIIA as promoters of metabolic dysfunction, particularly MASLD.