Key result
Metabolic pathways and inflammation synergistically drive venous thrombosis, highlighting the potential of anti-inflammatory strategies to reduce thrombotic risk.
Why the study?
Venous thrombosis involves a complex interplay between inflammation, coagulation, and platelet activation, with alterations in the metabolic microenvironment emerging as key drivers and potential risks for thrombotic disease.
This review highlights the synergistic interaction between metabolism, inflammation, and thrombosis in driving venous thrombotic disease, suggesting potential for anti-inflammatory therapeutic strategies.
Anti-inflammatory strategies merit testing in venous thrombosis; leaves open clinical efficacy pending prospective trials.
The findings of the last decade suggest a complex link between inflammatory cells, coagulation, and the activation of platelets and their synergistic interaction to promote venous thrombosis. Inflammation is present throughout the process of venous thrombosis, and various metabolic pathways of erythrocytes, endothelial cells, and immune cells involved in venous thrombosis, including glucose metabolism, lipid metabolism, homocysteine metabolism, and oxidative stress, are associated with inflammation. While the metabolic microenvironment has been identified as a marker of malignancy, recent studies have revealed that for cancer thrombosis, alterations in the metabolic microenvironment appear to also be a potential risk. In this review, we discuss how the synergy between metabolism and thrombosis drives thrombotic disease. We also explore the great potential of anti-inflammatory strategies targeting venous thrombosis and the complex link between anti-inflammation and metabolism. Furthermore, we suggest how we can use our existing knowledge to reduce the risk of venous thrombosis.
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Cao et al. (2024) conducted a review in Venous thrombosis. Metabolic pathways and anti-inflammatory strategies was evaluated. Metabolic pathways and inflammation synergistically drive venous thrombosis, highlighting the potential of anti-inflammatory strategies to reduce thrombotic risk.
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