{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T15:43:38Z","timestamp":1792597418851,"version":"4.5.0"},"reference-count":191,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2023,1,12]],"date-time":"2023-01-12T00:00:00Z","timestamp":1673481600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI162775"],"award-info":[{"award-number":["R21AI162775"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["R35GM142368"],"award-info":[{"award-number":["R35GM142368"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["WIREs Mechanisms of Disease"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The cyclic guanosine monophosphate\u2013adenosine monophosphate (GMP\u2010AMP) synthase\u2010Stimulator of Interferon Genes (cGAS\u2010STING) pathway is a critical innate immune mechanism for detecting the presence of double\u2010stranded DNA (dsDNA) and prompting a robust immune response. Canonical cGAS\u2010STING activation occurs when cGAS, a predominantly cytosolic pattern recognition receptor, binds microbial DNA to promote STING activation. Upon STING activation, transcription factors enter the nucleus to cause the production of Type I interferons, inflammatory cytokines whose primary function is to prime the host for viral infection by producing a number of antiviral interferon\u2010stimulated genes. While the pathway was originally described in viral infection, more recent studies have implicated cGAS\u2010STING signaling in a number of different contexts, including autoimmune disease, cancer, injury, and neuroinflammatory disease. This review focuses on how our understanding of the cGAS\u2010STING pathway has evolved over time with an emphasis on the role of STING\u2010mediated neuroinflammation and infection in the nervous system. We discuss recent findings on how STING signaling contributes to the pathology of pain, traumatic brain injury, and stroke, as well as how mitochondrial DNA may promote STING activation in common neurodegenerative diseases. We conclude by commenting on the current knowledge gaps that should be filled before STING can be an effective therapeutic target in neuroinflammatory disease.<\/jats:p>\n                  <jats:p>\n                    This article is categorized under:\n                    <jats:list list-type=\"simple\">\n                      <jats:list-item>\n                        <jats:p>Neurological Diseases &gt; Molecular and Cellular Physiology<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Infectious Diseases &gt; Molecular and Cellular Physiology<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>Immune System Diseases &gt; Molecular and Cellular Physiology<\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  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