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Peroxisome Proliferator–Activated Receptor α Gene Regulates Left Ventricular Growth in Response to Exercise and Hypertension
Author(s) -
Yalda Jamshidi,
Hugh Montgomery,
HansWerner Hense,
Saul Myerson,
Inès PinedaTorra,
Bart Staels,
Michael World,
Angela Doering,
Jeanette Erdmann,
Christian Hengstenberg,
Steve E. Humphries,
Heribert Schunkert,
David M. Flavell
Publication year - 2002
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/hc0802.104535
Subject(s) - medicine , endocrinology , left ventricular hypertrophy , muscle hypertrophy , allele , beta oxidation , peroxisome proliferator activated receptor , peroxisome , pathogenesis , cardiology , receptor , blood pressure , gene , biology , metabolism , genetics
Left ventricular hypertrophy (LVH) occurs as an adaptive response to a physiological (such as exercise) or pathological (valvular disease, hypertension, or obesity) increase in cardiac work. The molecular mechanisms regulating the LVH response are poorly understood. However, inherited defects in fatty acid oxidation are known to cause severe early-onset cardiac hypertrophy. Peroxisome proliferator--activated receptor alpha (PPARalpha) regulates genes responsible for myocardial fatty acid oxidation and is downregulated during cardiac hypertrophy, concomitant with the switch from fatty acid to glucose utilization.

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