http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2016237498-A1

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filingDate 2014-10-03-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_946ca928e3fd0f66eb1b0f3798e486fa
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_1b87d8c3efae7046bd5cfebd1a42c377
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publicationDate 2016-08-18-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-2016237498-A1
titleOfInvention Prediction and treatment of heart failure
abstract Chronic activation of the β-Adrenergic Receptor (β-AR) can have deleterious effects on the heart, and animal models over-expressing the β-AR develop heart failure. In the classical β-AR pathway, activation of the receptor results in increased cyclic AMP(cAMP) levels. However, β-ARs are desensitized in the failing heart and cAMP levels are decreased. Phosphodiesterase 3A (PDE3A) hydrolyzes cAMP in certain subcellular compartments in cardiac myocytes, regulating cAMP levels and subsequent protein kinase A mediated cell signaling. By virtue of being freely diffusable intracellularly and being reduced in failing myocardial tissue, cAMP is reduced in certain important cardiac myocyte subcellular compartments such as the microdomain occupied by phospholamban.
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Total number of triples: 2177.