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Mitochondrial DNA signals driving immune responses: Why, How, Where?
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Journal Article
Mitochondrial DNA signals driving immune responses: Why, How, Where?
2025
Overview
There has been a recent expansion in our understanding of DNA-sensing mechanisms. Mitochondrial dysfunction, oxidative and proteostatic stresses, instability and impaired disposal of nucleoids cause the release of mitochondrial DNA (mtDNA) from the mitochondria in several human diseases, as well as in cell culture and animal models. Mitochondrial DNA mislocalized to the cytosol and/or the extracellular compartments can trigger innate immune and inflammation responses by binding DNA-sensing receptors (DSRs). Here, we define the features that make mtDNA highly immunogenic and the mechanisms of its release from the mitochondria into the cytosol and the extracellular compartments. We describe the major DSRs that bind mtDNA such as cyclic guanosine-monophosphate-adenosine-monophosphate synthase (cGAS), Z-DNA-binding protein 1 (ZBP1), NOD-, LRR-, and PYD- domain-containing protein 3 receptor (NLRP3), absent in melanoma 2 (AIM2) and toll-like receptor 9 (TLR9), and their downstream signaling cascades. We summarize the key findings, novelties, and gaps of mislocalized mtDNA as a driving signal of immune responses in vascular, metabolic, kidney, lung, and neurodegenerative diseases, as well as viral and bacterial infections. Finally, we define common strategies to induce or inhibit mtDNA release and propose challenges to advance the field.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ AMP
/ Animals
/ Biology Beyond Boundaries: Mitochondrial and Cell Death in Translational Research
/ Biomedical and Life Sciences
/ Cellular signal transduction
/ Cytokines and Growth Factors
/ Cytosol
/ DNA, Mitochondrial - genetics
/ DNA, Mitochondrial - immunology
/ DNA, Mitochondrial - metabolism
/ Genomes
/ Humans
/ Melanoma
/ Proteins
/ Review
/ Z-form
