Table 1.

GPVI functions in inflammation. A non‐exhaustive list of the various effects of GPVI deficiency or blockade in models of inflammation. anti‐GBM: anti–glomerular basement membrane antibody; K/BxN serum: serum from K/BxN a mouse strain known to develop severe autoimmune inflammatory arthritis

Inflammation model	Effect of GPVI deficiency or blockade	References
Acute dermatitis (IgG immune‐complex mediated)	skin bleeding at the reaction site reduced platelet recruitment to the inflamed skin reduced reaction‐induced serotonin secretion	94, 102
Peritonitis (IgG immune‐complex mediated)	decreased MMP‐9 release in the peritoneal cavity no bleeding	94
Rheumatoid arthritis (K/BxN serum)	decreased vascular permeability in the inflamed joint decreased production of proinflammatory platelet microparticles	80, 84
Glomerulonephritis (anti‐GBM antibody)	reduced platelet recruitment to the inflamed glomerulus	99
Myocardial Ischemia‐Reperfusion (30 min long ligation of the left coronary artery)	reduced neutrophil recruitment reduced expression of inflammatory cytokines in the myocardium reduced microthrombosis improved microperfusion reduced infarct size intramyocardial bleeding	103, 104, 105
Cerebral Ischemia‐Reperfusion (60 min long occlusion of middle cerebral artery)	reduced infarct size reduced thrombosis in ischemic cortices improved microperfusion no bleeding	113, 116, 136
Lung infection (Klebsiella pneumoniae)	increased bacterial growth in infected lungs increased MMP‐9 release in the bronchoalveolar space increased inflammatory cytokines in the bronchoalveolar space reduced platelet recruitment and activation in the lung reduced platelet‐leukocyte complex formation in the lung minor bleeding	[148, 149]
Acute lung injury (LPS inhalation)	lung bleeding	102
Atherosclerosis (ApoE‐/‐ mice)	reduced platelet adhesion to atherosclerotic endothelium reduced atherosclerotic lesion formation	26, 33