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While the biochemical factors governing microglial activation are well understood, the impact of biophysical cues, such as extracellular matrix (ECM) mechanics, remains largely unexplored. Here, we demonstrate how matrix rigidity mechanoprimes microglia for inflammation through coordinated cytoskeletal\u2010to\u2010nuclear signaling and 3D spatio\u2010epigenomic remodeling. In response to rigid matrices, microglia undergo progressive actin cytoskeletal remodeling, morphological adaptation, and nuclear deformation. ATAC\u2010seq reveals that rigidity redistributes rather than globally increases chromatin accessibility: most differentially accessible regions lose accessibility, whereas a defined subset gains focal accessibility at inflammation\u2010associated loci, establishing a permissive state for subsequent activation. Upon LPS challenge, rigidity amplifies inflammatory responses through NF\u2010\u03baB activation and cytoskeleton\u2010dependent MRTF\u2010A nuclear translocation. Integrating ChIP\u2010seq and Hi\u2010C identifies rigidity\u2010responsive\n                    <jats:italic>cis<\/jats:italic>\n                    \u2010regulatory elements (mechanoCREs) and shows that rigidity promotes long\u2010range chromatin interactions linking distal mechanoCREs to inflammatory genes. Together, these findings establish ECM rigidity as a key regulator of microglial inflammation by coupling actin\u2010mediated mechanotransduction to chromatin accessibility and higher\u2010order genome organization, providing a mechanistic basis for mechanically amplified neuroinflammation.\n                  <\/jats:p>","DOI":"10.1002\/advs.77736","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T18:00:31Z","timestamp":1790532031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Matrix Rigidity Mechanoprimes Microglia for Inflammation Through Cytoskeletal\u2010to\u2010Nuclear Signaling and 3D Spatio\u2010Epigenomic Remodeling"],"prefix":"10.1002","author":[{"given":"Yu Xuan","family":"Meng","sequence":"first","affiliation":[{"name":"Institute of Tissue Regeneration Engineering (ITREN) Dankook University  Cheonan Republic of Korea"},{"name":"Institute of Toxicology, College of Preventive Medicine Third Military Medical University  Chongqing China"},{"name":"Department of Biological Sciences Korea Advanced Institute of Science and Technology (KAIST)  Daejeon Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaegeon","family":"Joo","sequence":"additional","affiliation":[{"name":"Department of Nanobiomedical Science &amp; 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