Open AccessHypertensive End-Organ Damage and Premature Mortality Are p38 Mitogen-Activated Protein Kinase–Dependent in a Rat Model of Cardiac Hypertrophy and Dysfunction
Author(s) -
Thomas M. Behr,
Sandhya S. Nerurkar,
Allen H. Nelson,
Robert W. Coatney,
Ti Woods,
Anthony C. Sulpizio,
Sudeep Chandra,
David P. Brooks,
Sanjay Kumar,
John C. Lee,
Eliot H. Ohlstein,
Christiane E. Angermann,
Jerry L. Adams,
Joseph Sisko,
Jonathan SacknerBernstein,
Robert N. Willette
Publication year - 2001
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/hc3601.094275
Subject(s) - medicine , endocrinology , muscle hypertrophy , mapk/erk pathway , p38 mitogen activated protein kinases , cardiology , kinase , biology , microbiology and biotechnology
Numerous pathological mediators of cardiac hypertrophy (eg, neurohormones, cytokines, and stretch) have been shown to activate p38 MAPK. The purpose of the present study was to examine p38 MAPK activation and the effects of its long-term inhibition in a model of hypertensive cardiac hypertrophy/dysfunction and end-organ damage.
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