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The mechanisms that enable the parasite to adapt its central carbon metabolism to the host's oxidative microenvironment remain poorly understood. Here, we report that oxidative stress serves as a key environmental cue that induces a profound metabolic rewiring. We identified pyruvate dehydrogenase kinase (EmPDK) as the central regulator governing this metabolic adjustment, favoring glycolysis and lactate production over oxidative phosphorylation (OXPHOS). Suppressing EmPDK activity enhances oxidative metabolism and impairs metacestode proliferation, whereas augmenting its function (via H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    \u2010induced upregulation) promotes glycolysis and growth. Reactive oxygen species (ROS) drive this metabolic reprogramming through the transcription factor EmHIF1\u03b1, forming an axis of ROS\/EmHIF1\u03b1\/EmPDK that modulates parasite metabolic plasticity. Our findings define EmPDK as a critical mediator of oxidative stress adaptation in\n                    <jats:italic>E. multilocularis<\/jats:italic>\n                    and support its further exploration as a candidate target for AE intervention.\n                  <\/jats:p>","DOI":"10.1002\/advs.76829","type":"journal-article","created":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T15:40:06Z","timestamp":1786635606000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Adaptation of\n                    <i>Echinococcus Multilocularis<\/i>\n                    to Oxidative Stress Depends on EmPDK\u2010Mediated Metabolic Reprogramming"],"prefix":"10.1002","volume":"13","author":[{"given":"Huijuan","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cellular Stress Biology School of Life Sciences Xiamen University  Xiamen Fujian China"},{"name":"Parasitology Research Laboratory 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