Key result
Human beta1-adrenergic receptor autoantibodies from patients with dilated cardiomyopathy potently stimulated ERK1/2 in murine cardiomyocytes via pathways distinct from classic beta-agonists.
Why the study?
Do beta1AR autoantibodies from DCM patients stimulate the ERK1/2 pathway in murine cardiomyocytes differently than classic beta-agonists?
Population
Murine cardiomyocytes and beta1-adrenergic receptor autoantibodies obtained from patients with idiopathic…
Comparison
beta1AR autoantibodies from DCM patients vs Classic beta-agonist isoproterenol
Design
Preclinical
Authors
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Distinct beta1AR autoantibody signaling may contribute to DCM pathogenesis; leaves open human relevance and therapeutic targeting.
Do beta1AR autoantibodies from DCM patients stimulate the ERK1/2 pathway in murine cardiomyocytes differently than classic beta-agonists?
Beta1AR autoantibodies from DCM patients activate ERK1/2 pathways in cardiomyocytes differently than classic beta-agonists, suggesting a distinct active receptor conformation that may contribute to heart failure pathogenesis.
Tutor et al. (2007) studied Idiopathic dilated cardiomyopathy (DCM). beta1-adrenergic receptor (beta1AR) autoantibodies vs. isoproterenol was evaluated on ERK1/2 activation in murine cardiomyocytes. Human beta1-adrenergic receptor autoantibodies from patients with dilated cardiomyopathy potently stimulated ERK1/2 in murine cardiomyocytes via pathways distinct from classic beta-agonists.
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