{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T05:03:59Z","timestamp":1779685439892,"version":"3.53.1"},"reference-count":105,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T00:00:00Z","timestamp":1779667200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Mitochondrial DNA (mtDNA) has long been recognized as an intracellular damage\u2212associated molecular pattern, but emerging evidence reveals its role as an intercellular messenger driving post\u2212infarction ventricular remodeling. This review systematically elaborates the transition of mtDNA from an \u201cintracellular DAMP\u201d to an \u201cintercellular messenger\u201d and proposes a conceptual framework termed the \u201cthree\u2212threshold model\u201d, which integrates existing evidence but requires direct experimental validation. The three thresholds are defined as the release threshold (mitophagy\u2212controlled mtDNA leakage), the transmission threshold (efficiency of intercellular transfer), and the activation threshold (sensitivity of STING signaling). mtDNA is transferred between cells via four modes\u2014naked mtDNA, Ambra1\n                    <jats:sup>+<\/jats:sup>\n                    sEVs, mt\u2212sEVs, and intact mitochondria\u2014mediating inflammation, fibrosis, and vascular dysfunction, respectively. These pathological effects continuously lower all three thresholds through positive feedback loops, driving irreversible remodeling. Time\u2212window\u2212based combination strategies offer a new paradigm for precision intervention. This framework integrates the entire process from mtDNA generation to intercellular transfer and downstream signaling, providing a systematic basis for precision intervention in post\u2212infarction remodeling. Importantly, several components of this model are based on preliminary or indirect evidence and await independent confirmation.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1852079","type":"journal-article","created":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T04:44:36Z","timestamp":1779684276000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial DNA-driven intercellular communication networks in post-infarction ventricular remodeling: the three-threshold model of cGAS-STING activation"],"prefix":"10.3389","volume":"17","author":[{"given":"Chao","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Xia","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiying","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiyi","family":"Tao","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuanchun","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yonghao","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Guang\u2019anmen Hospital, China Academy of Chinese Medical Sciences","place":["Beijing, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,25]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvae238","article-title":"PINK1-mediated mitophagy attenuates pathological cardiac hypertrophy by suppressing the mtDNA release-activated cGAS-STING pathway","volume":"121","author":"Zhou","year":"2025","journal-title":"Cardiovasc 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