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Catabolic Defect of Branched-Chain Amino Acids Promotes Heart Failure
Author(s) -
Haipeng Sun,
Kristine C. Olson,
Chen Gao,
Domenick A. Prosdocimo,
Meiyi Zhou,
Wang Zh,
Darwin Jeyaraj,
Ji-Youn Youn,
Shuxun Ren,
Yunxia Liu,
Christoph Rau,
Svati H. Shah,
Olga Ilkayeva,
W.J. Gui,
Noelle S. William,
Richard Wynn,
Christopher B. Newgard,
Hua Cai,
Xinshu Xiao,
David Chuang,
P. Christian Schulze,
Christopher J. Lynch,
Mukesh K. Jain,
Yibin Wang
Publication year - 2016
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.115.020226
Subject(s) - catabolism , pressure overload , branched chain amino acid , krüppel , heart failure , mitochondrion , amino acid , transcription factor , biochemistry , medicine , endocrinology , metabolism , biology , gene , leucine , cardiac hypertrophy
Although metabolic reprogramming is critical in the pathogenesis of heart failure, studies to date have focused principally on fatty acid and glucose metabolism. Contribution of amino acid metabolic regulation in the disease remains understudied.

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