The role of CCRL2 in the pathogenesis of experimental autoimmune myocarditis via PAK/NLRP3 pathway

In summary, we successfully constructed an EAM mice model and screened the DEGs based on bioinformatic analysis via transcriptome sequencing. The expression of CCRL2 had the highest level in EAM. CCRL2 knockdown alleviated EAM occurrence and suppressed PAK/NLRP3 expression. These results suggests that CCRL2 may act as a novel potential target in treatment of EAM through PAK1/NLRP3 pathway. However, the exact mechanisms involved in the regulation of EAM by CCRL2 via PAK1/NLRP3 still need to further study.