Table 1.

Targeting of Inflammasome Signaling in Preclinical Models of Venous Thrombosis

First Author (Ref. #)	Model	Inflammasome Signaling Inhibition Strategy	Main Findings
Gupta et al12	Rat IVC stenosis	NLRP3 siRNA Caspase-1 inhibition IL-1β inhibition	siRNA against NLRP3 and treatment with the caspase-1 inhibitor ac-YVAD-cmk or anti–IL-1β antibody reduced thrombus size, prothrombin/D-dimer levels, and platelet aggregability
Yadav et al15	Mouse IVC stenosis	IL-1 receptor antagonism IL-1β inhibition	Administration of an anti–IL-1β antibody or the IL-1 receptor antagonist anakinra decreased thrombus incidence and size without prolonging tail bleeding time
Li et al84	Rat IVC stenosis	IL-18 down-regulation	IL-18 down-regulation through lentiviral vectors suppressed venous thrombogenesis and the expression of NF-kB and vWF
Zhang et al13	Mouse IVC stenosis	Caspase-1-/- Caspase-11-/- GSDMD-/-	Deletion of caspase-1/GSDMD but not of caspase-11 reduced the incidence and extension of venous thrombosis
Campos et al14	Mouse IVC stenosis	Caspase-1 inhibition	Administration of the caspase-1 inhibitor ac-YVAD-cmk reduced the incidence of thrombosis as well as thrombus size and NETosis
Munzer et al11	Mouse IVC stenosis	NLRP3-/- Selective NLRP3 inhibition	NLRP3 inhibition with MCC950 in either mouse or human neutrophils diminished NETosis; NLRP3 deficiency reduced NETosis and thrombus progression
Abu-Fanne et al97	Mouse IVC stenosis	Nonselective NLRP3 inhibition	Colchicine treatment decreased clot size, and heparin coadministration reduced the heparin dose required to prevent thrombosis, with no discernable impact on hemostasis

GSDMD = gasdermin D; IVC = inferior vena cava; IL = interleukin; NF-kB = nuclear factor-kappa B; NLRP3 = NOD-, LRR-, and pyrin domain–containing protein 3; NETs = neutrophil extracellular traps; siRNA = small-interfering RNA; VWF = von Willebrand Factor.