In vitro studies using phenylephrine-treated neonatal rat ventricular myocytes, to explore the putative antihypertrophic effects of GDF11, showed that GDF11 did not reduce neonatal rat ventricular myocytes hypertrophy, but instead induced hypertrophy.Ĭardiovascular function can decline in old age, and the disease independent factors that induce these changes are not well known. There was no difference in myocyte cross-sectional area rGDF11 versus vehicle-treated old animals.

Ejection fraction, internal ventricular dimension, and septal wall thickness were not significantly different between rGDF11 and vehicle-treated animals at baseline and remained unchanged at 1, 2, and 4 weeks of treatment. Heart weight/body weight ratios of old mice were not different from 8- or 12-week-old animals, and the PCH marker atrial natriuretic peptide was not different in young versus old mice. After treatment, rGDF11 levels were significantly increased, but there was no significant effect on either heart weight or body weight. rGDF11 bioactivity was confirmed in vitro. Twenty-four–month-old C57BL/6 mice were given a daily injection of either recombinant (r) GDF11 at 0.1 mg/kg or vehicle for 28 days. Customer Service and Ordering Information.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).Here you will find options to view and activate subscriptions, manage institutional settings and access options, access usage statistics, and more.

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Pathological aging