| Predicate |
Object |
| assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_eb141b396e502bfce986c491d722e401
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_7830ef976413925cdd053f02c6a0995e |
| classificationCPCAdditional |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2333-916 |
| classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K45-06
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-50
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-5044
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C12Y305-01098 |
| classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-46 |
| filingDate |
2007-08-30-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_d88a8ee5e2c4d78ee3eab706a920b1b3 |
| publicationDate |
2008-03-06-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber |
WO-2008028065-A2 |
| titleOfInvention |
Sirt activation in managing heart failure |
| abstract |
Activation of a member of a class III histone deacetylase (e.g., SIRT1 and SIRT3) inhibits or blocks most of the events associated with heart failure (e.g., cardiomyocyte hypertrophy, cell death, loss of α-myosin isoform shift and fetal gene activation) and protects myocytes from hypertrophy agonist-mediated cell-death. SIRT1 and SIRT3 activation favors α-MHC expression and alters the myosin-isoform switch from β-MHC to α-MHC during cardiac hypertrophy. SIRT1 and SIRT3 activation negatively regulates cardiac hypertrophy and cell-phenotype, and these characteristics of SIRTs are therapeutically valuable for the treatment of heart failure. |
| isCitedBy |
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/EP-2214698-A2
http://rdf.ncbi.nlm.nih.gov/pubchem/patent/RU-2576512-C2 |
| priorityDate |
2006-08-31-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type |
http://data.epo.org/linked-data/def/patent/Publication |