7 results found
    1. Medicine

    Aorta smooth muscle-on-a-chip reveals impaired mitochondrial dynamics as a therapeutic target for aortic aneurysm in bicuspid aortic valve disease

    Mieradilijiang Abudupataer et al.
    An aorta smooth muscle-on-a-chip model indicated that NOTCH1 insufficiency in HAoSMCs induced phenotypic switching from a contractile to a synthetic phenotype accompanied by an impairment of mitochondrial fusion, implying its potential role as a therapeutic target for BAV-TAA.
    1. Developmental Biology

    A novel source of arterial valve cells linked to bicuspid aortic valve without raphe in mice

    Lorriane Eley et al.
    Identification of a novel source of progenitor cells that form arterial valve leaflets and that, when disrupted, can lead to bicuspid arterial valve, the most common human cardiac malformation.
    1. Developmental Biology

    Mechanically activated piezo channels modulate outflow tract valve development through the Yap1 and Klf2-Notch signaling axis

    Anne-Laure Duchemin et al.
    High resolution in vivo imaging of the zebrafish heart morphogenesis allows quantitative testing of the impact of stretch sensitive channels during outflow tract valve development.
    1. Medicine

    The tricuspid valve also maladapts as shown in sheep with biventricular heart failure

    William D Meador et al.
    Demonstrating the tricuspid valve maladapts is critical, and understanding its regurgitation may aid in developing better treatment strategies.
    1. Chromosomes and Gene Expression
    2. Medicine

    A deleterious gene-by-environment interaction imposed by calcium channel blockers in Marfan syndrome

    Jefferson J Doyle et al.
    Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.
    1. Developmental Biology

    Naa12 compensates for Naa10 in mice in the amino-terminal acetylation pathway

    Hyae Yon Kweon et al.
    Mice doubly deficient for Naa10 and Naa12 display embryonic lethality, with both enzymes compensating for each other with amino-terminal acetylation of proteins in mouse development.
    1. Developmental Biology

    Genetic dissection of Down syndrome-associated congenital heart defects using a new mouse mapping panel

    Eva Lana-Elola et al.
    A panel of seven new mouse strains with chromosomal duplications is used to identify a minimal genetic region required in three copies to cause congenital heart defects typical of human Down syndrome.

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