Molecular events underlying pregnancy-induced cardiomyopathy.
The etiology of cardiomyopathy in pregnant women remains unclear. In this issue, Hilfiker-Kleiner et al. (2007) report that a reduction in STAT3 and a concomitant increase in cathepsin D may be a cause of this disease. Cathepsin D generates an antiangiogenic cleavage product of the hormone prolactin. The authors show that an inhibitor of prolactin secretion may be useful in treating this disease.
Leinwand
Leslie A
LA
Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA. leinwand@colorado.edu
D000818:Animals; D001971:Bromocriptine / Q000627:therapeutic use; D009202:Cardiomyopathies / Q000188:drug therapy / Q000378:metabolism*; D002402:Cathepsin D / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism*; D011388:Prolactin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011644:Puerperal Disorders / Q000188:drug therapy / Q000378:metabolism*; D050796:STAT3 Transcription Factor / Q000378:metabolism*
D050796:STAT3 Transcription Factor; D001971:Bromocriptine; D011388:Prolactin; D002402:Cathepsin D