Open AccessHemin decreases cardiac oxidative stress and fibrosis in a rat model of systemic hypertension via PI3K/Akt signalling
Author(s) -
Morel E. Worou,
Karim Belmokhtar,
Pierre Bonnet,
Patrick Vourc’h,
M.-C. Machet,
Georges Khamis,
Véronique Eder
Publication year - 2011
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvr072
Subject(s) - hemin , oxidative stress , pi3k/akt/mtor pathway , protein kinase b , fibrosis , cardiac fibrosis , medicine , endocrinology , chemistry , microbiology and biotechnology , biology , signal transduction , biochemistry , heme , enzyme
Angiotensin II induces cardiac myocyte apoptosis and hypertrophy, which contribute to heart failure, possibly through enhanced oxidative stress. The aim of this work was to assess the impact of hemin (heme oxygenase-1 inducer) on NADPH oxidase activation, cardiac oxidative stress, and development of fibrosis in a rat model of renovascular hypertensive cardiomyopathy in comparison to an anti-hypertensive reference treatment with losartan.
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