|
Clinical setting | Animal model | Experimental outcome | References |
|
Atherosclerosis | mice | mice had smaller a plaque size compared to | Heller et al. [18] |
mice, CXCL10 antibody treatment | CXCL10 inhibition attenuated vulnerable plaque formation without size reduction compared to placebo | Segers et al. [19] |
mice, carotid artery cast model | Low shear stress increased CXCL10 mRNA tissue expression compared to normal shear stress | Cheng et al. [20] |
mice | mice had more stable plaques and smaller plaques compared to mice | Veillard et al. [21] |
mice, CXCR3 antagonist treatment | CXCR3 antagonist treatment attenuated vulnerable plaque formation and growth compared to placebo | Van Wanrooij et al. [22] |
mice | mice had a reduced plaque size compared to mice | Van Wanrooij et al. [23] |
|
Aneurysm formation | , angiotensin II infusion | mice had larger and more rupture-prone aneurysms compared to mice | King et al. [24] |
mice, Calcium Chloride infusion | mice had no reduction in aneurysm formation compared to wildtype mice | MacTaggart et al. [25] |
mice, Calcium Chloride infusion | mice had reduced aneurysm formation compared to wildtype mice | Gallo et al. [26] |
|
Myocardial infarction | Dogs, myocardial I/R | Upregulated CXCL10 mRNA expression 24–48 h after reperfusion in myocardial tissue |
Frangogiannis et al. [27] Dewald et al. [28] |
Wildtype mice, myocardial I/R | Upregulated CXCL10 mRNA expression 6 h after reperfusion in myocardial tissue | Dewald et al. [28] |
mice, myocardial I/R | mice had a reduced inflammatory, angiogenic, and fibrotic response compared to wildtype | Bujak et al. [29] |
|
Collateral artery formation | Wildtype mice, hindlimb ischemia | Upregulated CXCL10 mRNA expression in ischemic muscle tissue after hindlimb ischemia | Lee et al. [30], Waeckel et al. [31] |
mice, hindlimb ischemia | mice had a reduced perfusion recovery compared to wildtype mice | Van den Borne et al. [32] |
mice, hindlimb ischemia | mice had a reduced perfusion recovery compared to wildtype mice | Waeckel et al. [31] |
|
Clinical setting | Patient population | Clinical outcome | References |
|
Aneurysms | Thoracic aortic aneurysms | CXCL10 expression is correlated to outward remodeling and matrix degeneration | Tang et al. [33] |
Abdominal aortic versus popliteal artery aneurysm | Significant differences in CXCL10 expression levels between aneurysm subtypes |
Abdul-Hussien et al. [34] |
Thoracic aortic aneurysms (case-control study) | Higher circulating CXCL10 levels in cases versus controls | Gallo et al. [26] |
|
Coronary artery disease (CAD) | CAD | Higher baseline CXCL10 levels in cases versus controls, not predictive for CV risk | Herder et al. [35] |
CAD | Higher baseline CXCL10 levels in cases versus controls, no followup performed | Rothenbacher et al. [36] |
CAD | Higher baseline CXCL10 levels in cases versus controls, not predictive for CV risk | Ardigo et al. [37] |
Unstable angina | Higher CXCL10 expression in cases versus controls 6 h after complaints |
Oliveira et al. [38] |
Collateral formation | Increased collateral formation was associated with higher CXCL10 plasma levels | Keeley et al. [39] |
|
Myocardial infarction | Acute MI | Negative correlation between serum CXCL10 and markers for MI and infarct size | Koten et al. [40] |
Acute MI | Higher serum CXCL10 levels in acute MI patients versus healthy controls | Koten et al. [40] |
Acute MI | Positive correlation between serum CXCL10 levels and infarct size |
Ørn et al. [41] |
|
Peripheral artery disease (PAD) | Critical limb ischemia | Higher CXCL10 serum levels in patients versus controls | Teraa et al. [42] |
|