Marked enhancement in myocardial function resulting from overexpression of a human beta-adrenergic receptor gene.
Transgenic mice with intense cardiac expression of a human beta-adrenergic receptor gene were engineered and shown to display marked improvements in baseline myocardial and left ventricular function. Heart/body weight ratios and histologic appearance were not found to be significantly altered, suggesting that receptor gene expression did not induce pathologic changes. Given the substantial reduction in beta-adrenergic receptor density and resultant reduction in inotropic responsiveness observed in chronic heart failure, these findings represent a novel approach for increasing myocardial function with important clinical implications.
Milano, CA; Allen, LF; Dolber, PC; Johnson, TD; Rockman, HA; Bond, RA; Lefkowitz, RJ
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