Direct Renin Inhibition Exerts an Anti-hypertrophic Effect Associated with Improved Mitochondrial Function in Post-infarction Heart Failure in Diabetic Rats
Author(s) -
Rebecca ParodiRullán,
Giselle BarretoTorres,
Louis Ruiz,
José A. Casasnovas,
Sabzali Javadov
Publication year - 2012
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000178526
Subject(s) - aliskiren , heart failure , medicine , myocardial infarction , sirt3 , mitochondrion , ejection fraction , cardiac function curve , cardiology , endocrinology , infarction , ventricular remodeling , mitochondrial permeability transition pore , renin–angiotensin system , sirtuin , biology , apoptosis , programmed cell death , nad+ kinase , blood pressure , biochemistry , enzyme , microbiology and biotechnology
In addition to hypertension control, direct renin inhibition has been shown to exert direct beneficial effects on the heart in post-infarction cardiac remodeling. This study elucidates the possible contribution of mitochondria to the anti-hypertrophic effects of the direct renin inhibitor aliskiren in post-infarction heart failure complicated with diabetes in rats.
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