{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T01:12:04Z","timestamp":1790212324086,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"47","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"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"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Small"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Ferroptosis\u2010based cancer therapy shows promise in tumor suppression but is often limited by insufficient activation of antitumor immunity. Here, a hepatocellular carcinoma (HCC) targeted nanoplatform was constructed by coating FePDA nanozymes with Hepa1\u20106 cell membranes overexpressing ovalbumin (OVA) and CD40 ligand (CD40L), generating tumor membrane\u2010derived OVA\/CD40L\u2010functionalized FePDA nanoparticles (FePDA\u2010TMOC). This hybrid architecture integrates homologous tumor targeting with iron homeostasis disruption and co\u2010stimulatory immune activation within a single nanosystem. Mechanistically, the FePDA core induces sustained depletion of intracellular glutathione (GSH), leading to enhanced lipid peroxidation and promoting ferroptosis by disrupting the GPX4\u2010SLC7A11 axis. Simultaneously, the OVA\/CD40L\u2010modified membrane promotes efficient uptake by antigen\u2010presenting cells and enhances pro\u2010inflammatory immune activation through co\u2010stimulatory signaling. In vitro experiments demonstrated that FePDA\u2010TMOC selectively induces ferroptosis in Hepa1\u20106 cells and drives macrophage polarization toward a pro\u2010inflammatory phenotype. Following systemic administration, FePDA\u2010TMOC preferentially accumulates in tumors, markedly increases CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell infiltration, elevates pro\u2010inflammatory cytokine levels, and suppresses tumor growth and metastasis without observable systemic toxicity. By integrating ferroptosis induction with antitumor immune activation, this work highlights a rational strategy for transforming immune \u201ccold\u201d tumors into \u201chot\u201d tumors, providing a potential nanotherapeutic approach for HCC treatment.\n                  <\/jats:p>","DOI":"10.1002\/smll.74352","type":"journal-article","created":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T17:07:34Z","timestamp":1782925654000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Cell Membrane\u2010Engineered FePDA Nanoparticles Integrate Ferroptosis and Antitumor Immunity"],"prefix":"10.1002","volume":"22","author":[{"given":"Chongqing","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Immunology School of Basic Medical Sciences Anhui Medical University  Hefei 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