Table 1:

Key findings of PAI-1 in vascular remodeling, thrombosis, and cardiovascular diseases.

Reference	Aim of the study	Experimental strategy	Outcome
[81]	To investigate the effects of recombinant PAI-1 on intimal hyperplasia after intimal injury	Rats with carotid artery injury were injected mutant form of PAI-1 intraperitoneally and intimal hyperplasia was examined	Recombinant PAI-1 inhibits proteases and binding of VSMCs with vitronectin, thereby decreasing VSMCs migration. Recombinant PAI-1 attenuates intimal hyperplasia after intimal injury
[82]	To investigate the effects of PAI-1 on the mural, adaptive response to hypertension	Patients with essential hypertension and gender-matched normotensive patients had brachial intima-media thickness (IMT), flow-mediated dilation (FMD), and PAI-1 antigen in blood measured.	IMT and FMD correlated positively in hypertensive patients, FMD correlated inversely with wall stress, and IMT correlated inversely with PAI-1. This supports the hypothesis that PAI-1 attenuates increases in neointimal vascular smooth muscle cellularity
[83]	To investigate the hypothesis that PAI-1 inhibition prevents neointimal hyperplasia after arterial injury	A wire-injury model was made in WT and PAI-1 (−/−) mice. The mice were injected intraperitoneally with IMD-0354, an IKK inhibitor, and intimal hyperplasia was examined	Thickened intima was observed in WT arteries, while thickening was suppressed in PAI-1 (−/−) arteries. PAI-1 is an essential factor in the progression of vascular remodeling and its inhibition may prevent restenosis after arterial injury
[84]	To determine the vein wall response when exposed to increased and decreased plasmin activity	Stasis thrombi were created in a mouse IVC ligation model in uPA (−/−) and PAI-1 (−/−)	Thrombi were larger in uPA (−/−) mice and smaller in PAI-1 (−/−) mice with 8-day plasmin levels increased three-fold compared with WT. Therefore, plasmin activity is critical for thrombus resolution and PAI-1 plays a role in the prolongation of thrombi.
[85]	To investigate the role of the plasminogen activator system in coronary vascular remodeling during long-term nitric oxide synthase inhibition	WT, PAI-1 (−/−), and t-PA (−/−) mice were treated with N(omega)-nitro-L-arginine methyl ester (L-NAME)	PAI-1 deficiency protects against L-NAME-induced hypertension and perivascular fibrosis
[86]	To investigate the regulation of vein-graft (VG) thrombin activity by PAI-1	VGs from WT, PAI-1 (−/−), and PAI-1 transgenic mice were implanted into WT, PAI-1 (−/−), and PAI-1 transgenic arteries. VG remodeling was then assessed 4 weeks after.	Thrombin activity and thrombin-induced proliferation of PAI-1 deficient venous smooth muscle cells (SMCs) were significantly greater than that of WT SMCs. Thus challenging the hypothesis that PAI-1 drives non-thrombotic obstructive diseases.
[87]	To investigate the role of PAI-1 in the progression of venous thromboembolism (VTE) in pancreatic cancer patients	Plasma levels of PAI-1 were measured via ELISA in pancreatic cancer patients and mice bearing human tumors. The resolution of an acquired VTE was measured in the mice.	Mice bearing PANC-1 tumors had the highest levels of PAI-1 and exhibited impaired venous thrombus resolution 8 days after IVC stasis when compared with nontumor controls.
[88]	To investigate the specific determinants of clot lysis time (CLT)	Plasma levels of PAI-1, plasminogen, thrombin-activatable fibrinolysis inhibitor (TAFI), prothrombin, and α2-antiplasmin were measured in thrombosis patients and healthy control subjects.	After adjusting for acute-phase proteins, TAFI and PAI-1 remained associated with thrombosis.