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Dr. Dr. Tracks S100A1 alternative mechanism to enhance cardiac. Time is directly regulated which calcium circulation, which driven the contractions in the heart. Most lab was S100A1 part in hearts disease has worked over a decade, and with a group of out of Walter Koch, director of the Centre for Translational Medicine resulted, they have demonstrated fail that the loss of of said protein cause diseased heart and that the protein is a potential target in gene therapy for congestive heart failure.

The researchers plan still to study animal models of the hypertension and notes that the current study was simply a result of combined efforts of to those in the centers for Translational Medicine and possible well the Department of Physiology of. If the scientists found a deficiency of S100A1 has in the blood vessels, then they will to develop treatments the Centre in-house skills in order antiviral delivery, tailored for express Generated in endothelial cells of can be to generate. We will test genetic engineering animals to find out whether or not replacing or not replacing S100A1 lowering blood pressure, he says. – In addition, the scientists be testing a recently developed approach to about at only a small fragment of said protein with similar therapeutic potency This fragment . 10 is times less than the protein is and enables direct application of in the blood stream, just like a real medicine. Researchers hope is that either the tiny proteins fragment of yourself or a synthetic analogue of enable a new therapeutic approach to of both failure and treated high blood pressure patients in near future.