{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Newman LE"],"funding":["NIA NIH HHS","NCI NIH HHS","NIAMS NIH HHS","NIGMS NIH HHS","NIH HHS"],"pagination":["194-206"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11026068"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(2)"],"pubmed_abstract":["Mitochondrial DNA (mtDNA) encodes essential subunits of the oxidative phosphorylation system, but is also a major damage-associated molecular pattern (DAMP) that engages innate immune sensors when released into the cytoplasm, outside of cells or into circulation. As a DAMP, mtDNA not only contributes to anti-viral resistance, but also causes pathogenic inflammation in many disease contexts. Cells experiencing mtDNA stress caused by depletion of the mtDNA-packaging protein, transcription factor A, mitochondrial (TFAM) or during herpes simplex virus-1 infection exhibit elongated mitochondria, enlargement of nucleoids (mtDNA-protein complexes) and activation of cGAS-STING innate immune signalling via mtDNA released into the cytoplasm. However, the relationship among aberrant mitochondria and "],"journal":["Nature cell biology"],"pubmed_title":["Mitochondrial DNA replication stress triggers a pro-inflammatory endosomal pathway of nucleoid disposal."],"pmcid":["PMC11026068"],"funding_grant_id":["T32 GM007198","P30 AG068635","P30 CA014195","K99 GM141482","F32 GM137580","R00 CA245187","R01 AR069876","S10 OD023689"],"pubmed_authors":["Newman LE","Tadepalle N","Shadel GS","Weiser Novak S","Towers CG","Tremblay ME","Lemersal I","Rojas GR","Grotjahn DA","Rodriguez-Enriquez R","Donnelly MP","Ghosh S","Medina M","Schiavon CR","Chevez JA","Manor U","Rocha S"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial DNA replication stress triggers a pro-inflammatory endosomal pathway of nucleoid disposal.","description":"Mitochondrial DNA (mtDNA) encodes essential subunits of the oxidative phosphorylation system, but is also a major damage-associated molecular pattern (DAMP) that engages innate immune sensors when released into the cytoplasm, outside of cells or into circulation. As a DAMP, mtDNA not only contributes to anti-viral resistance, but also causes pathogenic inflammation in many disease contexts. Cells experiencing mtDNA stress caused by depletion of the mtDNA-packaging protein, transcription factor A, mitochondrial (TFAM) or during herpes simplex virus-1 infection exhibit elongated mitochondria, enlargement of nucleoids (mtDNA-protein complexes) and activation of cGAS-STING innate immune signalling via mtDNA released into the cytoplasm. However, the relationship among aberrant mitochondria and ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Feb","modification":"2025-04-04T01:36:02.09Z","creation":"2025-04-04T01:36:02.09Z"},"accession":"S-EPMC11026068","cross_references":{"pubmed":["38332353"],"doi":["10.1038/s41556-023-01343-1"]}}