Mitochondrial nucleic acids in innate immunity and beyond
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yoon, Jimin | - |
dc.contributor.author | Kim, Sujin | - |
dc.contributor.author | Lee, Mihye | - |
dc.contributor.author | Kim, Yoosik | - |
dc.date.accessioned | 2024-08-14T08:02:06Z | - |
dc.date.available | 2024-08-14T08:02:06Z | - |
dc.date.issued | 2023-12 | - |
dc.identifier.issn | 1226-3613 | - |
dc.identifier.issn | 2092-6413 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/26599 | - |
dc.description.abstract | Mitochondria participate in a wide range of cellular processes. One essential function of mitochondria is to be a platform for antiviral signaling proteins during the innate immune response to viral infection. Recently, studies have revealed that mitochondrion-derived DNAs and RNAs are recognized as non-self molecules and act as immunogenic ligands. More importantly, the cytosolic release of these mitochondrial nucleic acids (mt-NAs) is closely associated with the pathogenesis of human diseases accompanying aberrant immune activation. The release of mitochondrial DNAs (mtDNAs) via BAX/BAK activation and/or VDAC1 oligomerization activates the innate immune response and inflammasome assembly. In addition, mitochondrial double-stranded RNAs (mt-dsRNAs) are sensed by pattern recognition receptors in the cytosol to induce type I interferon expression and initiate apoptotic programs. Notably, these cytosolic mt-NAs also mediate adipocyte differentiation and contribute to mitogenesis and mitochondrial thermogenesis. In this review, we summarize recent studies of innate immune signaling pathways regulated by mt-NAs, human diseases associated with mt-NAs, and the emerging physiological roles of mt-NAs. Mitochondrial nucleic acids (mt-NAs) play a crucial role in activating various innate immune signaling pathways and are associated with numerous human diseases. Downregulation of mt-NAs or their downstream receptors often alleviates interferon signature. Recent studies reveal that mt-NAs can also serve as key mediators of signaling between mitochondria and the nucleus, thereby contributing to cell physiology. In particular, studies have shown that mt-NAs can stimulate beige adipocyte development in young mice, which has potential therapeutic implications for obesity and insulin resistance. Understanding the multifaceted roles of mt-NAs will provide potential therapeutic strategies for mt-NA-mediated immune signaling regulation in pathophysiology.This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | SPRINGERNATURE | - |
dc.title | Mitochondrial nucleic acids in innate immunity and beyond | - |
dc.type | Article | - |
dc.publisher.location | 영국 | - |
dc.identifier.doi | 10.1038/s12276-023-01121-x | - |
dc.identifier.scopusid | 2-s2.0-85178033752 | - |
dc.identifier.wosid | 001111472700006 | - |
dc.identifier.bibliographicCitation | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.citation.title | EXPERIMENTAL AND MOLECULAR MEDICINE | - |
dc.type.docType | Review; Early Access | - |
dc.identifier.kciid | ART003037469 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | DOUBLE-STRANDED-RNA | - |
dc.subject.keywordPlus | PERMEABILITY TRANSITION | - |
dc.subject.keywordPlus | DNA | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | RELEASE | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | ACTIVATE | - |
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