{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Schank M"],"funding":["NIH HHS"],"pagination":["1061"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10224005"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(5)"],"pubmed_abstract":["We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate the mechanism(s) of CD4 T cell mitochondrial compromise in ART-controlled PLWH. We first assessed the levels of reactive oxygen species (ROS), and we observed significantly increased cellular and mitochondrial ROS levels in CD4 T cells from PLWH compared to healthy subjects (HS). Furthermore, we observed a significant reduction in the levels of proteins responsible for antioxidant defense (superoxide dismutase 1, SOD1) and ROS-mediated DNA damage repair (apurinic/apyrimidinic endonuclease"],"journal":["Viruses"],"pubmed_title":["ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV."],"pmcid":["PMC10224005"],"funding_grant_id":["R21AI157909","R15AG069544","R15AG076370-01","R15AG076370-015S1"],"pubmed_authors":["Jiang Y","El Gazzar M","Ning S","Nguyen LNT","Moorman JP","Zhang J","Zhang Y","Yao ZQ","Wu XY","Zhao J","Schank M","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.","description":"We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate the mechanism(s) of CD4 T cell mitochondrial compromise in ART-controlled PLWH. We first assessed the levels of reactive oxygen species (ROS), and we observed significantly increased cellular and mitochondrial ROS levels in CD4 T cells from PLWH compared to healthy subjects (HS). Furthermore, we observed a significant reduction in the levels of proteins responsible for antioxidant defense (superoxide dismutase 1, SOD1) and ROS-mediated DNA damage repair (apurinic/apyrimidinic endonuclease","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Apr","modification":"2025-05-29T16:22:29.539Z","creation":"2025-05-29T16:22:29.539Z"},"accession":"S-EPMC10224005","cross_references":{"pubmed":["37243148"],"doi":["10.3390/v15051061"]}}