{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao X"],"funding":["National Natural Science Foundation of China"],"pagination":["879023"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9039263"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["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, an"],"journal":["Frontiers in cell and developmental biology"],"pubmed_title":["<i>Chlamydia pneumoniae</i> Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation."],"pmcid":["PMC9039263"],"funding_grant_id":["82070452 81700403"],"pubmed_authors":["Wang B","Zhang Y","Miao G","Zhang L","Xu Z","Zhao X","Zhao H"],"additional_accession":[]},"is_claimable":false,"name":"<i>Chlamydia pneumoniae</i> Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation.","description":"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, an","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-07-14T17:07:53.213Z","creation":"2025-04-05T11:07:38.352Z"},"accession":"S-EPMC9039263","cross_references":{"pubmed":["35493076"],"doi":["10.3389/fcell.2022.879023"]}}