{"id":"b20680d5af51","type":"article","url":"https://hartvaat.nl/2026/01/06/remming-van-annexine-a2-bevordert-mitofagie-en-vermindert-hartschade-na-infarct/","title":"Remming van annexine A2 bevordert mitofagie en vermindert hartschade na infarct","title_en":"Inhibition of Annexin A2 Facilitates PHB2-Mediated Mitophagy in Cardiomyocytes to Alleviate Cardiac Injury and Remodeling After Infarction","category":"algemeen","category_label":"Algemeen","professions":["cardioloog"],"tags":["myocardinfarct"],"journal":"Circulation","doi":"https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.077780","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.077780","authors":[],"significance":6,"published":"2026-01-06","source_date":"2026-01-06","image":"","kennis":[],"congress":"","summary_en":"This study demonstrated that inhibition of annexin A2 enhances mitophagy in cardiomyocytes and alleviates cardiac injury after myocardial infarction, identifying a new molecular target for cardioprotection.","created":"2026-07-03T10:25:35Z","updated":"2026-07-03T13:24:59Z","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":"Mitofagie is cruciaal bij hartschade en -herstel na een myocardinfarct. Dit onderzoek toont dat remming van annexine A2 de PHB2-gemedieerde mitofagie in cardiomyocyten bevordert, wat hartschade en remodeling na een infarct vermindert.","abstract_original":"BACKGROUND:Mitophagy is critically involved in cardiac injury and repair after myocardial infarction (MI), whereas the annexin A family plays an important role in mitophagy. However, the intrinsic molecular underpinnings that orchestrate the homeostasis of mitophagy in the infarcted heart remain to be fully characterized. Here, we aimed to evaluate the role of ANXA2 (annexin A2) in cardiac mitophagy in response to MI.METHODS:Transcriptome analyses were conducted to identify differentially expressed genes and enriched pathways. Mitophagy, mitochondrial function, and cardiac injury and remodeling were analyzed in MI mice and neonatal rat ventricular myocytes with cardiomyocyte-specific ANXA2 knockdown or overexpression, as well as in models with ANXA2 knockdown combined with PHB2 (prohibitin 2) silencing. Immunoprecipitation, mass spectrometry, and glutathione S-transferase pull-down assays were used to identify the interacting proteins of ANXA2.RESULTS:We showed that ANXA2 was highly ex"}