All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by inhibiting the renin-angiotensin system.

This study was designed to determine the effect of all-trans retinoic acid (RA) on the development of cardiac remodeling in a pressure overload rat model. Male Sprague-Dawley rats were subjected to sham operation and the aortic constriction procedure. A subgroup of sham control and aortic constricted rats were treated with RA for 5 mo after surgery.

Mitogen-activated protein kinases and mitogen-activated protein kinase phosphatases mediate the inhibitory effects of all-trans retinoic acid on the hypertrophic growth of cardiomyocytes.

All-trans retinoic acid (RA) has been implicated in mediation of cardiac growth inhibition in neonatal cardiomyocytes. However, the associated signaling mechanisms remain unclear. Utilizing neonatal cardiomyocytes, we demonstrated that RA suppressed the hypertrophic features induced by cyclic stretch or angiotensin II (Ang II).

PKC mediates cyclic stretch-induced cardiac hypertrophy through Rho family GTPases and mitogen-activated protein kinases in cardiomyocytes.

Signaling events, including Rho GTPases and protein kinase C (PKC), are involved in cardiac hypertrophy. However, the mechanisms by which these pathways cooperate during the hypertrophic process remain unclear. Using an in vitro cyclic stretch model with neonatal rat cardiomyocytes, we demonstrated that stretch-induced activation of RhoA, Rac1/Cdc42, and phosphorylation of Rho-guanine nucleotide dissociation inhibitor (GDI) were prevented by inhibition or depletion of PKC, using chelerythrine and phorbol 12-myristate 13-acetate, indicating that phorbol ester-sensitive PKC isozymes may be upstream regulators of Rho GTPases.

An aviator with cardiomyopathy and genetic susceptibility to hereditary hemochromatosis: a case report.

A 44-yr-old male pilot was diagnosed with non-ischemic cardiomyopathy, possibly as a complication of hereditary hemochromatosis, 8 yr after an acquired left bundle branch block was discovered on a routine ECG. Biochemical testing returned high levels of iron and percentage transferrin saturation, and genetic testing for hemochromatosis was remarkable for a heterozygous H63D mutation in the HFE gene on chromosome 6. Hereditary hemochromatosis should be considered in the differential diagnosis when a patient presents with cardiomyopathy and genetic testing for HFE gene variants influencing iron overload is now available as a clinical adjunct for diagnosis and patient management issues.