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Hippo and Cardiac Hypertrophy: A Complex Interaction.

08:00 EDT 23rd October 2015 | BioPortfolio

Summary of "Hippo and Cardiac Hypertrophy: A Complex Interaction."

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This article was published in the following journal.

Name: Circulation research
ISSN: 1524-4571
Pages: 832-4

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Medical and Biotech [MESH] Definitions

A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).

Autosomal dominant syndrome characterized by cardiac and cutaneous MYXOMAS; LENTIGINOSIS (spotty pigmentation of the skin), and endocrinopathy and its associated endocrine tumors. The cardiac myxomas may lead to SUDDEN CARDIAC DEATH and other complications in Carney complex patients. The gene coding for the PRKAR1A protein is one of the causative genetic loci (type 1). A second locus is at chromosome 2p16 (type 2).

An adaptor protein, consisting of seven WD REPEATS along its length, that functions as a component of the MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1 and MTORC2 COMPLEX. It interacts directly with MTOR to enhance its kinase activity and stabilizes the MTOR-RPTOR PROTEIN interaction in nutrient-poor conditions, favoring RPTOR inhibition of MTOR activity.

A cardiac arrhythmia that is caused by interaction of two independently initiated cardiac impulses of different rates from two separate foci. Generally one focus is the SINOATRIAL NODE, the normal pacemaker. The ectopic focus is usually in the HEART VENTRICLE but can be in the HEART ATRIUM or the ATRIOVENTRICULAR NODE. Modulation of the parasystolic rhythm by the sinus rhythm depends on the completeness of entrance block surrounding the parasystolic focus.

Diabetes complications in which VENTRICULAR REMODELING in the absence of CORONARY ATHEROSCLEROSIS and hypertension results in cardiac dysfunctions, typically LEFT VENTRICULAR DYSFUNCTION. The changes also result in myocardial hypertrophy, myocardial necrosis and fibrosis, and collagen deposition due to impaired glucose tolerance.

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