APJ ACTS AS A DUAL RECEPTOR IN CARDIAC HYPERTROPHY
@article{Scimia2012APJAA, title={APJ ACTS AS A DUAL RECEPTOR IN CARDIAC HYPERTROPHY}, author={M. C. Scimia and C. Hurtado and S. Ray and Scott Metzler and K. Wei and J. Wang and Chris E. Woods and N. Purcell and D. Catalucci and T. Akasaka and O. F. Bueno and G. Vlasuk and P. Kaliman and R. Bodmer and L. Smith and E. Ashley and M. Mercola and Joan Heller Brown and P. Ruiz-Lozano}, journal={Nature}, year={2012}, volume={488}, pages={394 - 398} }
Cardiac hypertrophy is initiated as an adaptive response to sustained overload but progresses pathologically as heart failure ensues. Here we report that genetic loss of APJ, a G-protein-coupled receptor, confers resistance to chronic pressure overload by markedly reducing myocardial hypertrophy and heart failure. In contrast, mice lacking apelin (the endogenous APJ ligand) remain sensitive, suggesting an apelin-independent function of APJ. Freshly isolated APJ-null cardiomyocytes exhibit an… CONTINUE READING
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Intervention | Other |
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