{"id":"097ea21fdfd6","type":"article","url":"https://hartvaat.nl/2025/12/18/endotheliale-transcriptiefactor-eb-beschermt-tegen-doxorubicine-cardiotoxiciteit/","title":"Endotheliale transcriptiefactor EB beschermt tegen doxorubicine-cardiotoxiciteit","title_en":"Endothelial Transcription Factor EB Protects Against Doxorubicin-Induced Endothelial Toxicity and Cardiac Dysfunction","category":"algemeen","category_label":"Algemeen","professions":["cardioloog"],"tags":["kanker-en-hart"],"journal":"Circulation","doi":"https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.124.071774","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.124.071774","authors":["Wa Du"],"significance":6,"published":"2025-12-18","source_date":"2025-12-18","image":"","kennis":["https://hartvaat.nl/kennis/cardiometabool/hart-en-kanker-cardio-oncologie/","https://hartvaat.nl/kennis/cardiometabool/insulineresistentie-mechanisme/"],"congress":"","summary_en":"This basic science study showed that endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction, identifying a potential therapeutic target for cardio-oncology.","created":"2026-07-03T10:25:40Z","updated":"2026-07-03T13:25:03Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Doxorubicine is een effectief chemotherapeuticum maar veroorzaakt cardiovasculaire toxiciteit. Endotheelceldisfunctie speelt een cruciale rol. Dit onderzoek toont dat endotheliale transcriptiefactor EB beschermt tegen doxorubicine-geïnduceerde toxiciteit en cardiale disfunctie.","abstract_original":"BACKGROUND:Doxorubicin (DOX), an effective chemotherapeutic drug for various cancers, has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell (EC) dysfunction is recognized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. TFEB (transcription factor EB), a master regulator of autophagy and lysosome biogenesis, regulates cardiovascular homeostasis. In the present study, we aimed to test whether endothelial TFEB protects against EC damage and alleviates cardiac dysfunction induced by DOX treatment.METHODS:EC-specific TFEB transgenic mice, EC-specific TFEB knockout mice, and their corresponding littermate controls were administered DOX intravenously. Survival curves were generated, and cardiac functions were measured in mice. The effects of TFEB on mitochondrial reactive oxygen species production, autophagic flux, and apoptosis were evaluated in human and mouse cardiac microvascular ECs treated with DOX. RNA sequ"}