{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T11:08:41Z","timestamp":1792494521786,"version":"4.5.0"},"reference-count":54,"publisher":"Wiley","issue":"51","license":[{"start":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T00:00:00Z","timestamp":1781481600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T00:00:00Z","timestamp":1781481600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100012246","name":"Priority Academic Program Development of Jiangsu Higher Education Institutions","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100012246","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Pancreatic cancer exhibits extensive metabolic reprogramming that supports rapid progression and therapeutic resistance, making metabolic vulnerabilities attractive targets for intervention. Here, a tumor microenvironment\u2010responsive nanoreactor (Pht@HMnO\n                    <jats:sub>2<\/jats:sub>\n                    \u2010HA) is designed to induce disulfidptosis in pancreatic cancer through coordinated metabolic interference and redox catalysis. Following CD44\u2010mediated tumor targeting and cellular internalization, the nanoreactor's responsive self\u2010optimization within the tumor microenvironment enables localized release of phloretin, suppressing glucose uptake and pentose phosphate pathway activity and thereby limiting intracellular reducing\u2010power generation. In parallel, the nanoreactor consumes intracellular glutathione and amplifies oxidative stress via MnO\n                    <jats:sub>2<\/jats:sub>\n                    \u2010mediated redox reactions, thereby depleting antioxidant defenses. Together, these processes impose reducing\u2010power deprivation and disrupt redox homeostasis, leading to cystine accumulation, disulfide stress, actin cytoskeleton collapse, and disulfidptosis in pancreatic cancer cells. Moreover, degradation\u2010associated Mn\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    release provides activatable T1\u2010weighted MRI contrast, enabling noninvasive visualization of intratumoral nanoreactor activation and therapeutic progression. Collectively, this work establishes a theranostic nanoreactor that exploits coupled metabolic and redox vulnerabilities to induce disulfidptosis, offering a mechanistically grounded strategy for precision therapy in pancreatic cancer.\n                  <\/jats:p>","DOI":"10.1002\/advs.76146","type":"journal-article","created":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T15:22:20Z","timestamp":1781536940000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Tumor Microenvironment\u2010Responsive Nanoreactor Induces Disulfidptosis in Pancreatic Cancer via Metabolic Interference and Redox Catalysis"],"prefix":"10.1002","volume":"13","author":[{"given":"Rui","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Radiology The First Affiliated Hospital of Soochow University  Suzhou China"},{"name":"State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and 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