1
Polyamines mediate acute metabolic effects and cardiac hypertrophy associated with β-adrenoceptor stimulation.
2
PS2KO mice developed normally with no evidence of cardiac hypertrophy and fibrosis.
3
Individual embryos were identified with cardiac hypertrophy as well as with hypoplasia.
4
FGF23 was also shown to induce cardiac hypertrophy directly acting on cardiomyocytes.
5
It also reduced cardiac hypertrophy and proteinuria developed in GB hypertensive rats.
6
Pathological cardiac hypertrophy is the main risk factor for heart diseases.
7
However, the effects of MRTF-A in cardiac hypertrophy remain poorly understood.
8
However, the treatments now used to decrease cardiac hypertrophy have had limited success.
9
However, the molecular mechanisms that regulate cardiac hypertrophy are largely unknown.
10
Results: GT reduced cardiac hypertrophy and improved systolic and diastolic dysfunction.
11
Echocardiography performed on three of four patients in group A revealed cardiac hypertrophy.
12
Some studies have suggested that microRNA-133a could reduce cardiac hypertrophy and myocardial fibrosis.
13
Endogenous polyamines mediate acute metabolic effects and cardiac hypertrophy associated to beta-adrenoceptor stimulation.
14
Pathological cardiac hypertrophy eventually leads to heart failure without adequate treatment.
15
The most striking morphological consequence of ablating GLUT4 is cardiac hypertrophy.
16
Perinatal DDT exposure induces hypertension and cardiac hypertrophy in adult mice.
