Molecular mechanisms of mitochondrial DNA release and activation of the cGAS-STING pathway
In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-ST...
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| Published in | Experimental & molecular medicine Vol. 55; no. 3; pp. 510 - 519 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.03.2023
Springer Nature B.V Nature Publishing Group 생화학분자생물학회 |
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| Online Access | Get full text |
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| Abstract | In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis.
Inflammatory diseases: Understanding mitochondrial DNA release
Cytosolic DNA activates the cGAS-STING pathway which mediates inflammation and antiviral response. One source of cytosolic DNA is ‘self ‘ DNA, such as mitochondrial DNA. Studies of how mitochondria can release DNA and trigger dangerous immune responses are revealing potential treatments for inflammatory diseases. Cells isolate DNA in their nuclei and mitochondria, but if this ‘self-DNA’ leaks out, it triggers the same immune responses that the body uses to fight DNA from viruses or bacteria. Jeonghan Kim at The Catholic University of Korea College of Medicine in Seoul, South Korea, and co-workers reviewed research into the mechanism causing mitochondrial DNA release, and the resulting inflammatory pathways. Although cGAS-STING is the central driver of such inflammation, treatments targeting it may also suppress the body’s antimicrobial immunity. A safer alternative maybe to inhibit mitochondrial VDAC oligomerization, which releases mitochondrial DNA. |
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| AbstractList | In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis.Inflammatory diseases: Understanding mitochondrial DNA releaseCytosolic DNA activates the cGAS-STING pathway which mediates inflammation and antiviral response. One source of cytosolic DNA is ‘self ‘ DNA, such as mitochondrial DNA. Studies of how mitochondria can release DNA and trigger dangerous immune responses are revealing potential treatments for inflammatory diseases. Cells isolate DNA in their nuclei and mitochondria, but if this ‘self-DNA’ leaks out, it triggers the same immune responses that the body uses to fight DNA from viruses or bacteria. Jeonghan Kim at The Catholic University of Korea College of Medicine in Seoul, South Korea, and co-workers reviewed research into the mechanism causing mitochondrial DNA release, and the resulting inflammatory pathways. Although cGAS-STING is the central driver of such inflammation, treatments targeting it may also suppress the body’s antimicrobial immunity. A safer alternative maybe to inhibit mitochondrial VDAC oligomerization, which releases mitochondrial DNA. In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis.In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis. In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis. In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis. KCI Citation Count: 0 Inflammatory diseases: Understanding mitochondrial DNA release Cytosolic DNA activates the cGAS-STING pathway which mediates inflammation and antiviral response. One source of cytosolic DNA is ‘self ‘ DNA, such as mitochondrial DNA. Studies of how mitochondria can release DNA and trigger dangerous immune responses are revealing potential treatments for inflammatory diseases. Cells isolate DNA in their nuclei and mitochondria, but if this ‘self-DNA’ leaks out, it triggers the same immune responses that the body uses to fight DNA from viruses or bacteria. Jeonghan Kim at The Catholic University of Korea College of Medicine in Seoul, South Korea, and co-workers reviewed research into the mechanism causing mitochondrial DNA release, and the resulting inflammatory pathways. Although cGAS-STING is the central driver of such inflammation, treatments targeting it may also suppress the body’s antimicrobial immunity. A safer alternative maybe to inhibit mitochondrial VDAC oligomerization, which releases mitochondrial DNA. In addition to constituting the genetic material of an organism, DNA is a tracer for the recognition of foreign pathogens and a trigger of the innate immune system. cGAS functions as a sensor of double-stranded DNA fragments and initiates an immune response via the adaptor protein STING. The cGAS-STING pathway not only defends cells against various DNA-containing pathogens but also modulates many pathological processes caused by the immune response to the ectopic localization of self-DNA, such as cytosolic mitochondrial DNA (mtDNA) and extranuclear chromatin. In addition, macrophages can cause inflammation by forming a class of protein complexes called inflammasomes, and the activation of the NLRP3 inflammasome requires the release of oxidized mtDNA. In innate immunity related to inflammasomes, mtDNA release is mediated by macropores that are formed on the outer membrane of mitochondria via VDAC oligomerization. These macropores are specifically formed in response to mitochondrial stress and tissue damage, and the inhibition of VDAC oligomerization mitigates this inflammatory response. The rapidly expanding area of research on the mechanisms by which mtDNA is released and triggers inflammation has revealed new treatment strategies not only for inflammation but also, surprisingly, for neurodegenerative diseases such as amyotrophic lateral sclerosis. Inflammatory diseases: Understanding mitochondrial DNA release Cytosolic DNA activates the cGAS-STING pathway which mediates inflammation and antiviral response. One source of cytosolic DNA is ‘self ‘ DNA, such as mitochondrial DNA. Studies of how mitochondria can release DNA and trigger dangerous immune responses are revealing potential treatments for inflammatory diseases. Cells isolate DNA in their nuclei and mitochondria, but if this ‘self-DNA’ leaks out, it triggers the same immune responses that the body uses to fight DNA from viruses or bacteria. Jeonghan Kim at The Catholic University of Korea College of Medicine in Seoul, South Korea, and co-workers reviewed research into the mechanism causing mitochondrial DNA release, and the resulting inflammatory pathways. Although cGAS-STING is the central driver of such inflammation, treatments targeting it may also suppress the body’s antimicrobial immunity. A safer alternative maybe to inhibit mitochondrial VDAC oligomerization, which releases mitochondrial DNA. |
| Author | Kim, Ho-Shik Kim, Jeonghan Chung, Jay H. |
| Author_xml | – sequence: 1 givenname: Jeonghan orcidid: 0000-0003-1695-9630 surname: Kim fullname: Kim, Jeonghan email: jhk@catholic.ac.kr organization: Department of Biochemistry, The Catholic University of Korea College of Medicine – sequence: 2 givenname: Ho-Shik orcidid: 0000-0003-2121-6655 surname: Kim fullname: Kim, Ho-Shik organization: Department of Biochemistry, The Catholic University of Korea College of Medicine – sequence: 3 givenname: Jay H. surname: Chung fullname: Chung, Jay H. email: chungj@nhlbi.nih.gov organization: Laboratory of Obesity and Aging Research, Cardiovascular Branch, National Heart Lung and Blood Institute, National Institutes of Health |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36964253$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART002947633$$DAccess content in National Research Foundation of Korea (NRF) |
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| SubjectTerms | Amyotrophic lateral sclerosis Antiviral drugs Biomedical and Life Sciences Biomedicine Chromatin DNA viruses DNA, Mitochondrial - genetics DNA, Mitochondrial - metabolism Humans Immune response Immunity, Innate Inflammasomes Inflammasomes - metabolism Inflammation Inflammation - metabolism Inflammatory diseases Innate immunity Localization Macrophages Medical Biochemistry Membrane Proteins - metabolism Mitochondria Mitochondria - metabolism Mitochondrial DNA Molecular Medicine Molecular modelling Neurodegenerative diseases Nucleotidyltransferases - genetics Oligomerization Pathogens Review Article Signal Transduction Stem Cells 생화학 |
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| Title | Molecular mechanisms of mitochondrial DNA release and activation of the cGAS-STING pathway |
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