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    Home > Food News > Nutrition News > New research on cardiac atrophy lays the foundation for preventing damage from long-term space flights

    New research on cardiac atrophy lays the foundation for preventing damage from long-term space flights

    • Last Update: 2021-08-06
    • Source: Internet
    • Author: User
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    Image: Scientists at Cincinnati Children's Hospital have discovered a molecular pathway that can trigger potentially fatal cardiac atrophy


    Source: Cincinnati Children

    In many cases, cardiomyocytes do not respond to external pressure like skeletal muscle cells


    The new findings based on the study of mouse models represent an important milestone in long-term efforts to prevent or even reverse cardiac atrophy


    "NASA is very interested in cardiac atrophy," said Dr.


    Since doctors discovered many years ago that astronauts returning to Earth are usually barely able to walk, astronauts have been exercising in orbit to minimize the loss of muscle mass


    The new findings of Morkentin and his colleagues help explain why muscle atrophy also affects the heart, which in turn provides potential new ways to prevent or treat this problem


    A three-pronged attack on heart cells

    The research team studied mouse models in several ways to track the atrophy of heart cells to a three-step molecular process


    Just like skeletal muscle, the heart increases or decreases as the workload increases


    The overexpression of thrombospondin-1 in the mouse heart directly activates a signaling protein called PERK, resulting in a rapid and fatal loss of heart quality, called atrophy


    The longer these genes are active, the more severe the atrophy will become


    "Our findings describe a new pathway for muscle mass loss," said Morkentin


    Next step

    Researchers still need to confirm that the processes observed in mice also occur in humans


    In humans, although we lack the ability to replace lost myocardial tissue, it should be possible to restore weakened or atrophied cardiomyocytes to their original state



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