{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T13:42:50Z","timestamp":1793281370830,"version":"4.5.0"},"reference-count":178,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T00:00:00Z","timestamp":1785110400000},"content-version":"vor","delay-in-days":26,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100031312","name":"Justis- og beredskapsdepartementet","doi-asserted-by":"publisher","award":["2023BAA005"],"award-info":[{"award-number":["2023BAA005"]}],"id":[{"id":"10.13039\/100031312","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Stroke remains a major global cause of death and disability, with many patients either missing the therapeutic window or responding poorly to current first\u2010line treatments. Consequently, secondary neurological injury, driven predominantly by neuroinflammation, has emerged as a critical therapeutic target. Microglia rapidly sense post\u2010stroke microenvironmental changes and adopt distinct inflammatory phenotypes that shape pathophysiological outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Accumulating evidence, including high\u2010resolution spatial profiling and single\u2010cell omics, positions mitochondrial dysfunction at the core of these responses. This review synthesizes recent findings on microglial mitochondrial dysfunction in stroke, introducing the concept of a microglial mitochondrial \u201cstorm center\u201d. In this model, reactive oxygen species (ROS) trigger an inflammatory cascade, while impairments in mitochondrial quality control (MQC) exacerbate pathogenic signaling. Metabolic reprogramming further sustains inflammatory polarization, influencing interactions with neurons, astrocytes, and endothelial cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This \u201cstorm center\u201d provides a conceptual framework for developing strategies to mitigate secondary brain injury. Finally, this review highlights key molecular mechanisms, potential therapeutic targets, and translational opportunities, providing a stronger foundation for future stroke research and therapeutic innovation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.71060","type":"journal-article","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T22:35:28Z","timestamp":1785191728000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Microglial Mitochondrial Dysfunction: The Storm Center of Post\u2010Stroke Neuroinflammation"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-4549-7456","authenticated-orcid":false,"given":"Ruchong","family":"Fan","sequence":"first","affiliation":[{"name":"Department of Neurology, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology  Wuhan Hubei 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