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Apelin and APJ orchestrate complex tissue-specific control of cardiomyocyte hypertrophy and contractility in the hypertrophy-heart failure transition
The G protein-coupled receptor APJ is a promising therapeutic target for heart failure. Constitutive deletion of APJ in the mouse is protective against the hypertrophy-heart failure transition via elimination of ligand-independent, β-arrestin-dependent stretch transduction. However, the cellular ori...
Tallennettuna:
| Julkaisussa: | Am J Physiol Heart Circ Physiol |
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| Päätekijät: | , , , , , , , , , , , , , , |
| Aineistotyyppi: | Artigo |
| Kieli: | Inglês |
| Julkaistu: |
American Physiological Society
2018
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| Aiheet: | |
| Linkit: | https://ncbi.nlm.nih.gov/pmc/articles/PMC6139625/ https://ncbi.nlm.nih.gov/pubmed/29775410 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1152/ajpheart.00693.2017 |
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