{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen S"],"funding":["Chinese Institutes for Medical Research","2022 Chronic disease prevention and health education research project","National Natural Science Foundation of China","Beijing Hospitals Authority Youth Programme","Key Projects of the Beijing Municipal Education Commission's Science and Technology Plan","Beijing Municipal Administration of Hospitals Incubating Program","High-level public health technical personnel construction Project","Talent Cultivation plan of \"Climbing the peak\" of Beijing Municipal Hospital Administration","Beijing Natural Science Foundation-Changping Innovation Joint Fund","Beijing You'an Hospital Construction of Talent Pool Program","Training Fund for Open Projects at Clinical Institutes and Departments of Capital Medical University"],"pagination":["246"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11657569"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["30(1)"],"pubmed_abstract":["<h4>Background</h4>Acetaminophen (APAP)-induced acute liver injury (AILI) is the most prevalent cause of acute liver failure and mitochondrial dysfunction plays a dominant role in the pathogenesis of AILI. Mitochondrial transcription factor A (TFAM) is an important marker for maintaining mitochondrial functional homeostasis, but its functions in AILI are unclear. This study aimed to investigate the function of TFAM and its regulatory molecular mechanism in the progression of AILI.<h4>Methods</h4>The roles of TFAM and DEAD (Asp-Glu-Ala-Asp) box polypeptide 3 X-linked (DDX3X) in AILI were determined with TFAM overexpression and DDX3X knockdown, respectively.<h4>Results</h4>TFAM expression was suppressed in AILI patients. TFAM overexpression alleviated liver necrosis and mitochondrial dysfunc"],"journal":["Molecular medicine (Cambridge, Mass.)"],"pubmed_title":["Depressed TFAM promotes acetaminophen-induced hepatotoxicity regulated by DDX3X-PGC1α-NRF2 signaling pathway."],"pmcid":["PMC11657569"],"funding_grant_id":["BJMB0012022028021","CX24PY23","KZ202010025035","Subject leaders-02-13","L234046","DFL20221503","82002243, 82100653","PX2021065","CCMU2023ZKYXZ003","QML20201702","YARCKB2022008"],"pubmed_authors":["Xu L","Pan Z","Ren F","Fan Z","Wei Q","Liu M","Cao Y","Tian Y","Zhang X","Gao Y","Chen S","Wei L"],"additional_accession":[]},"is_claimable":false,"name":"Depressed TFAM promotes acetaminophen-induced hepatotoxicity regulated by DDX3X-PGC1α-NRF2 signaling pathway.","description":"<h4>Background</h4>Acetaminophen (APAP)-induced acute liver injury (AILI) is the most prevalent cause of acute liver failure and mitochondrial dysfunction plays a dominant role in the pathogenesis of AILI. Mitochondrial transcription factor A (TFAM) is an important marker for maintaining mitochondrial functional homeostasis, but its functions in AILI are unclear. This study aimed to investigate the function of TFAM and its regulatory molecular mechanism in the progression of AILI.<h4>Methods</h4>The roles of TFAM and DEAD (Asp-Glu-Ala-Asp) box polypeptide 3 X-linked (DDX3X) in AILI were determined with TFAM overexpression and DDX3X knockdown, respectively.<h4>Results</h4>TFAM expression was suppressed in AILI patients. TFAM overexpression alleviated liver necrosis and mitochondrial dysfunc","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2025-04-04T01:54:31.447Z","creation":"2025-04-04T01:54:31.447Z"},"accession":"S-EPMC11657569","cross_references":{"pubmed":["39701936"],"doi":["10.1186/s10020-024-01017-0"]}}