{
  "abstract": "Mitoxyperilysis is a proposed lytic death pathway in which oxidatively damaged mitochondria become membrane-lethal when retained at the plasma membrane. In founding models, TLR stimulation plus carbon restriction engaged MYD88-dependent innate signalling and BAX/BAK1/BID-dependent mitochondrial oxidative stress, while mTORC2–RhoA–actin remodelling prolonged peripheral mitochondrial retention. Mitoxyperiosis denotes prolonged mitochondria-plasma membrane association and localised oxidative membrane injury, whereas mitoxyperilysis denotes the subsequent plasma membrane rupture and lytic cell death. In these models, NINJ1 contributed to terminal rupture and LDH/HMGB1 release without being required for cell death. The damaging oxidant, physical tether, and mechanism linking local injury to membrane failure remain unresolved. Sepsis may reproduce upstream metabolic-redox conditions, but direct evidence for the complete spatial sequence in patient-derived cells is lacking. This review separates founding-model findings from disease-relevant observations and untested steps.",
  "abstract_shown": true,
  "affiliations": [
    "Rehabilitation Department, The People’s Hospital Medical Group of Xiangzhou",
    "Department of Intensive Care Unit, The People’s Hospital Medical Group of Xiangzhou"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Yu Zhang"
    },
    {
      "affs": [
        0
      ],
      "name": "Xin Ping Xia"
    },
    {
      "affs": [
        1
      ],
      "name": "Ling Zhao"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/eehw5setbsp5h.bib",
  "cited_by": 0,
  "doi": "10.3389/fimmu.2026.1991494",
  "fulltext_url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991494/full",
  "id": "eehw5setbsp5h",
  "issns": [
    "1664-3224"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991494/full",
  "language": "en",
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "lcc",
      "RC581-607"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-04",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/eehw5setbsp5h.ris",
  "sources": [
    {
      "first_seen": "2026-11-04T12:21:26Z",
      "native_id": "10.3389/fimmu.2026.1991494",
      "source": "crossref",
      "url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991494/full"
    },
    {
      "first_seen": "2026-11-04T14:20:54Z",
      "native_id": "00b8a1761b2148c6849fdf8b3bdb5d55",
      "source": "doaj",
      "url": "https://doi.org/10.3389/fimmu.2026.1991494"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "issn:1664-3224",
      "subfield": "immunology"
    },
    {
      "field": "medicine",
      "origin": "lcc:RC581-607",
      "subfield": "general"
    }
  ],
  "title": "When location makes oxidative stress lethal: mitoxyperilysis at the immunometabolic stress interface",
  "title_text": "When location makes oxidative stress lethal: mitoxyperilysis at the immunometabolic stress interface",
  "type": "peer-reviewed",
  "updated_at": "2026-11-06T14:20:20Z",
  "url": "https://research.draconitic.com/paper/eehw5setbsp5h",
  "venue": "Frontiers in Immunology",
  "versions": []
}