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In addition to the decisive role in thrombosis, platelets play an important role in the immediate response to vascular injury by promoting vascular inflammation, immunomodulation and atherosclerosis. The complement system is a critical part of the innate immune response, promoting homeostasis and causing dysfunction of tissues. It has been suggested as a promising therapeutic target for restoring tissue function in myocardial infarction according to recent clinical and preclinical studies. Controversy exists regarding the role of the complement receptor C5aR1 in angiogenesis. Some studies have suggested that C5aR1 has a proangiogenic effect, but others have suggested that it has an inhibitory effect on neovascularisation.
Our previous results have shown that the deficiency of platelet-specific C5aR1 gene leads to a proangiogenic phenotype with increased collateralisation, capillarisation and pericyte coverage in a hindlimb ischemia mouse model. Tissue neovascularisation could be controlled by activation of the C5a/C5aR1 axis in platelets and subsequent induction of the antiangiogenic factor CXCL4. Disruption of the C5aR1-CXCL4 axis reverses the antiangiogenic effects of platelets in vitro and in vivo.
The effects of platelet C5a/C5aR1 signaling on vascular regulation, as well as its involvement in additional processes during myocardial infarction, will be further explored in our future studies.