This review uncovers how interferon-gamma contributes to thrombosis and highlights its potential as a target for treatment.
IFN-γ, a key player in the pathogenesis of deep vein thrombosis (DVT), acts as a bridge between immune responses and coagulation activation. It promotes endothelial activation, leukocyte recruitment, cytokine release, and coagulation imbalance. This critical pro-inflammatory and prothrombotic role makes IFN-γ a promising molecular target in DVT management beyond traditional anticoagulation methods. Exploring pharmacological inhibition of IFN-γ signaling or its downstream effectors could open new therapeutic pathways for DVT, enhancing resolution and averting post-thrombotic complications. This review summarizes pathophysiology, diagnostics, and management of DVT, and adds further information on the role of IFN-γ as a key cytokine to target to advance DVT therapeutics.
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Kawaljit Kaur (2025) studied this question.
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