New Class of Therapy for Chronic Heart Failure

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Identifier new_class_therapy_chronic_heart_failure
Title New Class of Therapy for Chronic Heart Failure
Creator Shaw, R. M. U of U Health Key Faculty Collaborator: Hong, T.; Internal Medicine; School of Medicine; University of Utah Health
Subject Diffusion of Innovation; Heart Failure; Myocytes, Cardiac; Intracellular Signaling Peptides and Proteins; Hydrocortisone; Stress, Physiological; Myocardial Bridging; Biomarkers; Genetic Therapy; Knowledge Discovery
Keyword Cardiovascular
Image Caption Schematic illustration of microdomain organization of the structural protein BIN-1 within t-tubules of the adult ventricular cardiomyocytes. Originally published in Physiol Rev. 2017 January;97(1):227.
Description In the US, heart failure affects approximately eight million people, carries a poor prognosis, and represents the single largest healthcare cost for people over 65 years old. Most heart failure therapies rely on blocking the deleterious effects of stress hormones on the heart, but therapies aimed at repairing failing heart muscles are lacking. The lab directed by Robin Shaw (MD, PhD) and Nora Eccles Harrison Cardiovascular Research & Training Institute (CVRTI) Investigators have identified an architectural protein (cBIN1) of heart muscle cells that organizes the intracellular signalizing network responsible for heart muscle contraction and relaxation. They found that lowering cBIN1 caused heart failure progression, and that, in animal models, replacement of cBIN1 by gene therapy rescued failing heart muscle and prevented death. Furthermore, they devised a cBIN1 blood test that can predict hospitalization and death caused by heart failure in patients. Shaw and his team are now preparing for preclinical development of a cBIN1-directed therapy for heart failure. Successful development of such a therapy will significantly improve the lives of Americans and economics of our health care system.
Relation is Part of 2020
Publisher Spencer S. Eccles Health Sciences Library, University of Utah
Date Digital 2021
Date 2020
Type Image
Format image/jpeg
Rights Management Copyright © 2021, University of Utah, All Rights Reserved
Language eng
ARK ark:/87278/s6md4zzw
References 1.) Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia. Hong, T., et al., Nat Med, 2014 June;20(6):624. 2.) Plasma BIN1 correlates with heart failure and predicts arrhythmia in patients with arrhythmogenic right ventricular cardiomyopathy. Hong, T.T., et al., Heart Rhythm. 2012 June;9(6):961. 3.) BIN1 is reduced and Cav1.2 trafficking is impaired in human failing cardiomyocytes. Hong, T.T., et al., Heart Rhythm. 2012 May;9(5):812. 4.) BIN1 localizes the L-type calcium channel to cardiac T-tubules. Hong, T.T., et al., PLoS Biol. 2010 February 16; 8(2):e1000312. 5.) Association of a novel diagnostic biomarker, the plasma cardiac bridging integrator 1 score, with heart failure with preserved ejection fraction and cardiovascular hospitalization. Nikolova, A.P., et al., JAMA Cardiol. 2018 December 1;3(12):1206. 6.) In mice subjected to chronic stress, exogenous cBIN1 preserves calcium-handling machinery and cardiac function. Liu, Y., et al., JACC Basic Transl Sci. 2020 May 13;5(6):561. 7.) The ESCRT-III pathway facilitates cardiomyocyte release of cBIN1-containing microparticles. Xu, B., et al., PLoS Biol. 2017 August 14;15(8):e2002354. 8.) cBIN1 score (cs) identifies ambulatory HFrEF patients and predicts cardiovascular events. Hitzeman, T.C., et al., Front Physiol. 2020 May 25;11:503.
Setname ehsl_50disc
ID 1703461
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