Targeting Endoglin, an Auxiliary TGF-β Coreceptor, to Prevent Fibrosis and Heart Failure
Over the past 25 years, cardiovascular medicine has witnessed substantial progress in our understanding of the molecular pathogenesis, genetic etiologies as well as in the design of more efficacious therapeutic interventions. These advances have resulted in the dramatic reduction in the mortality of heart disease, especially in industrialized societies. Notwithstanding, both the prevalence and incidence of heart failure remain staggeringly high, posing new challenges and opportunities for prevention, diagnosis and management. Defined as the inability of the heart, as a mechanical pump, to meet the peripheral metabolic demands, this syndrome has many complex pathophysiological interactions among systolic performance, ventricular relaxation, impairments of contractility, and diastolic dysfunction. Both acquired (i.e., acute myocardial infarction) and genetic factors (mutations in genes encoding structural proteins) contribute to this clinical pathology but the development of overt heart failure ominously increases morbidity and decreases life-span. (SELECT FULL TEXT TO CONTINUE)
- Received May 1, 2012.
- Accepted May 2, 2012.
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