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Maternal androgen excess induces cardiac hypertrophy and left ventricular dysfunction in female mice offspring.
Molecular regulation of cardiac hypertrophy. Int J Biochem Cell Biol 2008; 40: 2023-2039, doi: 10.1016/j.biocel.2008.02.020.
Inhibition of NF-[kappa]B activity in the hypothalamic paraventricular nucleus attenuates hypertension and cardiac hypertrophy by modulating cytokines and attenuating oxidative stress.
Several other studies have illustrated that NT-proBNP is associated with functional status and progression of cardiac hypertrophy.2 The diagnostic utility data of NT-proBNP regarding left ventricle hypertrophy due to aortic regurgitation is very limited but it is demonstrated that NT-proBNP is increased during disease severity.
Cardiac hypertrophy has long been known as an independent risk factor for cardiac morbidity and all-cause mortality.[1],[2] It is an adaptive mechanism which is beneficial in the short term.
Greater handgrip strength was associated with less cardiac hypertrophy and remodelling, which are indicators of long-term cardiovascular disease.
Cardiac hypertrophy was induced using Phenylephrine (PE) and Isoprotenol (ISO).
The development of hyperinsulinemia and insulin resistance in murine cardiac hypertrophy is due to pressure overload boosts in myocardial insulin signalling to Akt (in excess), which adds to left ventricular reconstruction at an accelerated level and ultimately, a shift to heart failure [65].
In the article titled "Inducible Conditional Vascular-Specific Overexpression of Peroxisome Proliferator-Activated Receptor Beta/Delta Leads to Rapid Cardiac Hypertrophy" [1], there are errors in Figures 1, 2, and 5.
Evidences suggest that H3K27me3 is an important factor for cardiac hypertrophy [12] and generation of ROS [13, 14].
In the article "Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice" [1], there was an error in Figure 1(a), where the IL-22, [beta]-MHC, and GAPDH bands were triplicated, due to a production error.
In response to hypertension or other pressure overload diseases, cardiac hypertrophy occurs, resulting in enlargement of cell size, enrichment of cell number, or both.
(2008), demonstrated that the use of miR-21 antagonists in rats with concentric cardiac hypertrophy induced by pressure overload, significantly reduced remodeling, improving systolic function.
Green tea shows promise of preventing cardiac hypertrophy secondary to kidney failure.