{"id":"b4d0a773aa50","type":"article","url":"https://hartvaat.nl/2026/02/06/trpm7-deficientie-beschermt-tegen-myocardiale-ischemie-reperfusieschade/","title":"TRPM7-deficiëntie beschermt tegen myocardiale ischemie-reperfusieschade","title_en":"TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular Zn2+ Homeostasis","category":"algemeen","category_label":"Algemeen","professions":["cardioloog"],"tags":["acuut-hartfalen","hypertrofische-cardiomyopathie"],"journal":"Circulation","doi":"https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.074791","source_url":"https://doi.org/https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.125.074791","authors":["Xin Li"],"significance":6,"published":"2026-02-06","source_date":"2026-02-06","image":"","kennis":["https://hartvaat.nl/kennis/cardiometabool/diabetes-en-cardiovasculair-risico/","https://hartvaat.nl/kennis/cardiometabool/hart-en-kanker-cardio-oncologie/"],"congress":"","summary_en":"This study showed that TRPM7 channel deficiency protects against myocardial ischemia-reperfusion injury by regulating intracellular zinc homeostasis, identifying a potential therapeutic target for reducing reperfusion damage.","created":"2026-07-03T10:25:24Z","updated":"2026-07-03T13:24:49Z","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":"Ischemische hartziekte is een belangrijke doodsoorzaak. Reperfusie is noodzakelijk maar veroorzaakt paradoxale celdood. Dit onderzoek toont dat TRPM7-deficiëntie beschermt tegen ischemie-reperfusieschade door regulatie van intracellulaire zinkhomeostase.","abstract_original":"BACKGROUND:Ischemic heart disease is one of the leading causes of death worldwide. Timely reperfusion is necessary for myocardium salvage but triggers paradoxical cardiomyocyte death and contributes to up to 50% of the final infarct size, known as lethal ischemia/reperfusion (I/R) injury. TRPM7 (transient receptor potential melastatin 7) is a divalent cation–permeable, nonselective channel kinase that can sense oxidative stress and release Zn2+from unique intracellular TRPM7 vesicles. However, the pathophysiological role of intracellular TRPM7 remains poorly understood.METHODS:TRPM7 expression was determined in hearts from patients with ischemic heart failure and I/R-injured mice. Global cardiomyocyte-specific (cmTrpm7−/−) and fibroblast-specific (fibTrpm7−/−)Trpm7knockout mice were used to determine the role of TRPM7 in I/R injury. Mechanistic investigations were conducted in primary neonatal mouse cardiomyocytes and human induced pluripotent stem cell–derived cardiomyocytes with patc"}