Mitochondrial DNA in innate immune responses and inflammatory pathology
By A. West, G. Shadel. Nature reviews. Immunology, 2017
972 citations recorded by the source corpus.
Mitochondrial DNA (mtDNA) — which is well known for its role in oxidative phosphorylation and maternally inherited mitochondrial diseases — is increasingly recognized as an agonist of the innate immune system that influences antimicrobial responses and inflammatory pathology. On entering the cytoplasm, extracellular space or circulation, mtDNA can engage multiple pattern-recognition receptors in cell-type- and context-dependent manners to trigger pro-inflammatory and type I interferon responses. Here, we review the expanding research field of mtDNA in innate immune responses to highlight new mechanistic insights and discuss the physiological and pathological relevance of this exciting area of mitochondrial biology.
Subfields: Education
View Paper: https://www.semanticscholar.org/paper/5db3276cd1d382e74abe67410831bbd51424d581
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Citations in the corpus
- BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis (2018, background): “Indeed, whether and how herniation may be triggered during HIV or dengue infection, calcium overload, irradiation, or during inflammatory diseases such as systemic lupus erythematosus or rheumatoid arthritis—all conditions that have been associated with loss of mtDNA from the matrix (13, 69, 70)— re”
- LINE-1 derepression in senescent cells triggers interferon and inflammaging (2019, neutral): “Cytoplasmic DNA can originate from several sources, such as mtDNA released from stressed mitochondria 28 or cytoplasmic chromatin fragments (CCF) released from damaged nuclei 29,30 .”