A20 or tumor necrosis factor-induced protein 3 is a negative regulator of nuclear factor kappaB signaling. A20 has been shown previously to attenuate cardiac hypertrophy in vitro and postmyocardial infarction remodeling in vivo. In the present study, we tested the hypothesis that overexpression of A20 in the murine heart would protect against cardiac hypertrophy in vivo. The effects of constitu...

introduction: hypertrophied tonsils and adenoids may cause upper airway obstruction and cardio-pulmonary complications due to pulmonary arterial hypertension. the aim of this study was to determine the correlation between mean pulmonary arterial pressure (mpap) and selected adenotonsilar hypertrophy indexes. materials and methods: thirty two patients with upper-airway obstruction resulting from...

Cardiac hypertrophy in response to multiple stimuli has important physiological and pathological significances. GATA4 serves as a nuclear integrator of several signalling pathways during cardiac hypertrophy. Sp1 and Sp3 are also reported to be involved in this process. However, the mechanism by which GATA4 acts as a mediator, integrating these ubiquitously expressed transcriptional factors, is ...

Protein kinase D (PKD) is a nodal point in cardiac hypertrophic signaling. It triggers nuclear export of class II histone deacetylase (HDAC) and regulates transcription. Although this pathway is thought to be critical in cardiac hypertrophy and heart failure, little is known about spatiotemporal aspects of PKD activation at the myocyte level. Here, we demonstrate that in adult cardiomyocytes tw...

A20 or tumor necrosis factor–induced protein 3 is a negative regulator of nuclear factor B signaling. A20 has been shown previously to attenuate cardiac hypertrophy in vitro and postmyocardial infarction remodeling in vivo. In the present study, we tested the hypothesis that overexpression of A20 in the murine heart would protect against cardiac hypertrophy in vivo. The effects of constitutive ...

There is substantial evidence supporting a hypertrophic action of serotonin [5-hydroxytryptamine (5-HT)] in cardiomyocytes. However, little is known about the mechanisms involved. We previously demonstrated that 5-HT-induced hypertrophy depends, in part, on the generation of reactive oxygen species by monoamine oxidase-A (MAO-A) (see Ref. 3). Cardiomyocytes express 5-HT(2) receptors, which may ...

Activation of the nuclear factor κB (NF-κB) signaling pathway may be associated with the development of cardiac hypertrophy and transition to heart failure (HF). The transgenic mouse, MyoTg, develops hypertrophy and HF as a result of overexpression of myotrophin in the heart associated with elevated level of NF-κB activity. Using this mouse model and an NF-κB-targeted gene array, we first deter...

Pathological cardiac hypertrophy was produced by partial abdominal aortic constriction (PAAC) for 4 wk, while physiological cardiac hypertrophy was produced by chronic swimming training (CST) for 8 wk in rats. Pentoxifylline (30 mg/kg, 300 mg/kg i.p., day-1) treatment was started three days before PAAC and CST and it was continued for 4 wk in PAAC and 8 wk in CST experimental model. The left ve...

background: the association of metabolic syndrome (ms) with left  ventricular (lv) hypertrophy is controversial. the objective of our study was to investigate the infl uence of ms on lv mass and geometry in community-based hypertensive patients among han chinese.materials and methods: this study included 1733 metabolic syndrome patients according to the international diabetes federation (idf) d...

To improve contractile function, the myocardium undergoes hypertrophic growth without myocyte proliferation in response to both pathologic and physiologic stimulation. Various membrane-bound receptors and intermediate signal transduction pathways regulate the induction of cardiac hypertrophy, but the cardioprotective regulatory pathways or effectors that antagonize cardiac hypertrophy remain po...