And the decreases in the expressions of Fra-1, JunB and MMP2 in VSMCs were approximately 79.92%, 91.01% and 92.95% in the infected ApoE‐/‐TLR2‐/‐ mice compared with ApoE‐/‐ mice with C. pneumoniae infection (Figures 8C–H), suggesting that TLR2/mtROS/JunB-Fra-1/MMP2 signal axis plays a crucial role in C. pneumoniae infection-induced atherosclerosis development. Here, FOSL1 is linked to atherosclerosis.