Molecular insight into how a heart failure drug in clinical trials works
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Individuals who have persistent high blood pressure are at increased risks of a number of serious medical conditions, including heart failure.
One of the factors that contributes to such heart failure is thickening of the muscle wall of the heart. Such thickening (known as hypertrophy) is a compensatory response of the heart to the high blood pressure. A team of researchers at Johns Hopkins University, Baltimore, has provided new insight into both the signaling mechanisms by which high blood pressure leads to compensatory hypertrophy of the mouse heart and the molecular mechanisms by which a heart failure drug in clinical trials works.
In the study, which was led by Eiki Takimoto and David Kass, when mice lacking the protein RGS2 were manipulated such that they had persistent high blood pressure they developed hypertrophy of the muscle wall of the heart more rapidly than normal mice manipulated in the same way. Further, these mice went on to exhibit heart failure and died at a young age. Additional analysis indicated that a drug that prevents hypertrophy by targeting the protein PDE5 was less effective at preventing hypertrophy caused by high blood pressure in RGS2-deficient mice than in normal mice. These data have clinical implications, as they provide insight into the mechanism by which PDE5 inhibitors, which have recently entered clinical trials to treat a form of heart failure, work.
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Dr Andrew Whitten, Dr Cy Jeffries and Professor Jill Trewhella, from the School of Molecular and Microbial Biosciences, University of Sydney, with Samantha Harris, from the University of California, USA, have the first data showing how a protein in heart muscle cells works to maintain regular heart function. The research, published in the Proceedings of
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For the first time, researchers have found that a modified form of a naturally occurring protein, N-cadherin, could prevent blocked arteries. Blocked arteries are a major cause of heart attacks and strokes. The thickening of the artery wall, which occurs due to the build-up of fat and cells in the artery wall leads to
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A new clinical trial suggests that long-term use of candesartan, a drug currently used to treat hypertension, may significantly reduce the symptoms of genetic heart disease. The related report by Penicka et al, “The effects of candesartan on left ventricular hypertrophy and function in non-obstructive hypertrophic cardiomyopathy: a pilot, randomized study,” appears in the January
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