biostudies-literatureZhao XNational Natural Science Foundation of China879023https://www.ebi.ac.uk/biostudies/studies/S-EPMC9039263biostudies-literatureUnknown10Infection is closely related to atherosclerosis, which is a major pathological basis for cardiovascular diseases. Vascular smooth muscle cell (VSMC) migration is an important trigger in development of atherosclerosis that is associated with <i>Chlamydia pneumoniae</i> (<i>C. pneumoniae</i>) infection. However, the mechanism of VSMC migration remains unclear, and whether antioxidant could be a therapeutic target for <i>C. pneumoniae</i> infection-induced atherosclerosis also remains unknown. The results showed that <i>C. pneumoniae</i> infection mainly impaired mitochondrial function and increased the level of mitochondrial reactive oxygen species (mtROS). The expressions of protein JunB, Fra-1 and Matrix metalloproteinase 2 (MMP) evidently increased after <i>C. pneumoniae</i> infection, anFrontiers in cell and developmental biology<i>Chlamydia pneumoniae</i> Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation.PMC903926382070452 81700403Wang BZhang YMiao GZhang LXu ZZhao XZhao Hfalse<i>Chlamydia pneumoniae</i> Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation.Infection is closely related to atherosclerosis, which is a major pathological basis for cardiovascular diseases. Vascular smooth muscle cell (VSMC) migration is an important trigger in development of atherosclerosis that is associated with <i>Chlamydia pneumoniae</i> (<i>C. pneumoniae</i>) infection. However, the mechanism of VSMC migration remains unclear, and whether antioxidant could be a therapeutic target for <i>C. pneumoniae</i> infection-induced atherosclerosis also remains unknown. The results showed that <i>C. pneumoniae</i> infection mainly impaired mitochondrial function and increased the level of mitochondrial reactive oxygen species (mtROS). The expressions of protein JunB, Fra-1 and Matrix metalloproteinase 2 (MMP) evidently increased after <i>C. pneumoniae</i> infection, an2022-01-01T00:00:00Z20222026-07-14T17:07:53.213Z2025-04-05T11:07:38.352ZS-EPMC90392633549307610.3389/fcell.2022.879023