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    Home > Biochemistry News > Biotechnology News > The Organelle Homeostasis and Disease Research Group of the Institute of Zoology collaborated to discover the mechanism by which the mitochondrial outer membrane protein FUNDC2 mediates doxorubicin-induced ferroptosis and myocardial injury

    The Organelle Homeostasis and Disease Research Group of the Institute of Zoology collaborated to discover the mechanism by which the mitochondrial outer membrane protein FUNDC2 mediates doxorubicin-induced ferroptosis and myocardial injury

    • Last Update: 2022-09-07
    • Source: Internet
    • Author: User
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    Doxorubicin is a broad-spectrum antitumor drug currently in clinical use, and has therapeutic effects on a variety of tumors


    On August 29, 2022, Liu Lei's group from the Institute of Zoology, Chinese Academy of Sciences and Chen Yu's group from Nankai University jointly published a paper entitled "Mitochondrial outer membrane protein FUNDC2 promotes ferroptosis and contributes to doxorubicin (DOX)-induced cardiomyopathy in the journal PNAS.


    The study found that although the FUNDC2 protein was highly expressed in the heart, the FUNDC2 knockout mice had normal heart function


    In conclusion, this study focused on the regulation of mitochondrial outer membrane protein FUNDC2 on doxorubicin-induced ferroptosis and cardiomyopathy, and revealed the molecular mechanism of the FUNDC2-SLC25A11 axis involved in ferroptosis by regulating mitochondrial GSH amount; this study will help to further understand mitochondrial ferroptosis The relationship between homeostasis and ferroptosis and related diseases provides new ideas for the prevention and treatment of related diseases


    Dr.


     

    Figure 1 Schematic diagram of FUNDC2-mediated doxorubicin-induced ferroptosis and cardiomyopathy

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