http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2022275105-A1

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filingDate 2020-07-31-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_8957a700b0849d0e16d6649d9dd56576
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publicationDate 2022-09-01-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-2022275105-A1
titleOfInvention Neutralizing granzyme b for providing cardioprotection in a subject who experienced a myocardial infarction
abstract A method for providing cardioprotection in a subject who experienced a myocardial infarction, including administering a therapeutically effective amount of a Granzyme B inhibitor. Following acute MI in mice, CD8+ T lymphocytes are quickly recruited and activated in ischemic heart tissue, and release Granzyme B, leading to cardiomyocyte apoptosis and deterioration of myocardial function. Antibody-mediated depletion of CD8+ T lymphocytes decreases Granzyme B content and apoptotic within the myocardium and inflammatory response. mAb mediated-CD8 depletion limits myocardial injury and improves heart function. These effects are recapitulated in mice with CD8+ T cell selective Granzyme B deficiency in mice. Granzyme B is produced by other cell types (e.g., NK cells). Global Granzyme B deletion (GzmB-/- mice) decreases apoptotic within the myocardium, reduces local pro-inflammatory signature and ultimately limits infarct size after MI. Elevated circulating levels of Granzyme B in patients with acute MI predict increased risk of death after 1 year.
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Total number of triples: 535.