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Iron derived from autophagy-mediated ferritin degradation induces cardiomyocyte death and heart failure in mice

التفاصيل البيبلوغرافية
العنوان: Iron derived from autophagy-mediated ferritin degradation induces cardiomyocyte death and heart failure in mice
المؤلفون: Jumpei Ito, Shigemiki Omiya, Mara-Camelia Rusu, Hiromichi Ueda, Tomokazu Murakawa, Yohei Tanada, Hajime Abe, Kazuki Nakahara, Michio Asahi, Manabu Taneike, Kazuhiko Nishida, Ajay M Shah, Kinya Otsu
المصدر: eLife, Vol 10 (2021)
بيانات النشر: eLife Sciences Publications Ltd, 2021.
سنة النشر: 2021
المجموعة: LCC:Medicine
LCC:Science
LCC:Biology (General)
مصطلحات موضوعية: autophagy, iron, necrosis, ferritin, heart failure, Medicine, Science, Biology (General), QH301-705.5
الوصف: Heart failure is a major public health problem, and abnormal iron metabolism is common in patients with heart failure. Although iron is necessary for metabolic homeostasis, it induces a programmed necrosis. Iron release from ferritin storage is through nuclear receptor coactivator 4 (NCOA4)-mediated autophagic degradation, known as ferritinophagy. However, the role of ferritinophagy in the stressed heart remains unclear. Deletion of Ncoa4 in mouse hearts reduced left ventricular chamber size and improved cardiac function along with the attenuation of the upregulation of ferritinophagy-mediated ferritin degradation 4 weeks after pressure overload. Free ferrous iron overload and increased lipid peroxidation were suppressed in NCOA4-deficient hearts. A potent inhibitor of lipid peroxidation, ferrostatin-1, significantly mitigated the development of pressure overload-induced dilated cardiomyopathy in wild-type mice. Thus, the activation of ferritinophagy results in the development of heart failure, whereas inhibition of this process protects the heart against hemodynamic stress.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2050-084X
Relation: https://elifesciences.org/articles/62174; https://doaj.org/toc/2050-084X
DOI: 10.7554/eLife.62174
URL الوصول: https://doaj.org/article/d7ee8c4057a14ed1a17e5078bbd36987
رقم الأكسشن: edsdoj.7ee8c4057a14ed1a17e5078bbd36987
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:2050084X
DOI:10.7554/eLife.62174