Open AccessHuman Apolipoprotein A-I Gene Transfer Reduces the Development of Experimental Diabetic Cardiomyopathy
Author(s) -
Sophie Van Linthout,
Frank Spillmann,
Alexander Riad,
Christiane Trimpert,
Joke Lievens,
Marco Meloni,
Felicitas Escher,
Elena Filenberg,
Okan Demir,
Jun Li,
Mehdi Shakibaei,
Ingolf Schimke,
Alexander Staudt,
Stephan B. Felix,
HeinzPeter Schultheiß,
Bart De Geest,
Carsten Tschöpe
Publication year - 2008
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.710830
Subject(s) - diabetic cardiomyopathy , medicine , endocrinology , apolipoprotein b , streptozotocin , contractility , oxidative stress , inflammation , cardiomyopathy , ex vivo , fibrosis , diabetes mellitus , in vivo , cholesterol , biology , heart failure , microbiology and biotechnology
The hallmarks of diabetic cardiomyopathy are cardiac oxidative stress, intramyocardial inflammation, cardiac fibrosis, and cardiac apoptosis. Given the antioxidative, antiinflammatory, and antiapoptotic potential of high-density lipoprotein (HDL), we evaluated the hypothesis that increased HDL via gene transfer (GT) with human apolipoprotein (apo) A-I, the principal apolipoprotein of HDL, may reduce the development of diabetic cardiomyopathy.
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