CONCLUSIONS Taken together, these results suggest that BBR inhibits CVB3 replication through the suppression of JNK and p38 MAPK activation, shedding new light on the investigation of therapeutic strategies against CVB3-induced viral myocarditis.
Our results show a direct relationship between CAR and p38 MAPK levels, and since the p38 MAPK inhibitor treatment resulted in reduced levels of CAR as well as lower inflammatory infiltration, it is possible that the signaling pathway may mediate CAR expression during the pathogenesis of VMC.