Pressure-overload stress to the heart causes pathological cardiac hypertrophy, which increases the risk of cardiac morbidity and mortality. However, the detailed signaling pathways induced by pressure overload remain unclear. Here we used phosphoproteomics to delineate signaling pathways in the myocardium responding to acute pres-sure overload and chronic hypertrophy in mice. Myocar-dial samples at 4 time points (10, 30, 60 min and 2 weeks) after transverse aortic banding (TAB) in mice underwent quantitative phosphoproteomics assay. Temporal phos-phoproteomics profiles showed 360 phosphorylation sites with significant regulation after TAB. Multiple mechanical stress sensors were activated after acute pressure over-load. Gene ontology analys...
Abstract Cardiac hypertrophy provides an adaptive mechanism to maintain cardiac output in response t...
In response to chronic hypertension, the heart compensates by hypertrophic growth, which frequently ...
To study the role of early energetic abnormalities in the subsequent development of heart failure, w...
Pressure-overload stress to the heart causes pathological cardiac hypertrophy, which increases the r...
Pressure overload (POL) is a classical model for studying cardiac hypertrophy, but there has been no...
<div><p>Small animal models of afterload stress have contributed much to our present understanding o...
Phospholamban (PLN) plays a central role in Ca2+ homeostasis in cardiac myocytes through regulation ...
Abstract—Pressure overload has been shown to induce mitogen activated protein kinases (MAPKs) and re...
Peroxisome proliferator-activated receptor alpha (PPARalpha) regulates lipid metabolism at the trans...
<p><b>A</b>: BP recordings; Representative recording was shown from 5 mice; <b>B</b>: Echocardiograp...
AbstractCardiac hypertrophy is an important risk factor for cardiac morbidity and mortality. To unra...
Reversible protein phosphorylation is a posttranslational modification of regulatory proteins involv...
Pressure overload has been shown to induce mitogen activated protein kinases (MAPKs) and reactivate ...
Cardiac hypertrophy is an important risk factor for cardiac morbidity and mortality. To unravel the ...
Reversible protein phosphorylation is a posttranslational modification of regulatory proteins involv...
Abstract Cardiac hypertrophy provides an adaptive mechanism to maintain cardiac output in response t...
In response to chronic hypertension, the heart compensates by hypertrophic growth, which frequently ...
To study the role of early energetic abnormalities in the subsequent development of heart failure, w...
Pressure-overload stress to the heart causes pathological cardiac hypertrophy, which increases the r...
Pressure overload (POL) is a classical model for studying cardiac hypertrophy, but there has been no...
<div><p>Small animal models of afterload stress have contributed much to our present understanding o...
Phospholamban (PLN) plays a central role in Ca2+ homeostasis in cardiac myocytes through regulation ...
Abstract—Pressure overload has been shown to induce mitogen activated protein kinases (MAPKs) and re...
Peroxisome proliferator-activated receptor alpha (PPARalpha) regulates lipid metabolism at the trans...
<p><b>A</b>: BP recordings; Representative recording was shown from 5 mice; <b>B</b>: Echocardiograp...
AbstractCardiac hypertrophy is an important risk factor for cardiac morbidity and mortality. To unra...
Reversible protein phosphorylation is a posttranslational modification of regulatory proteins involv...
Pressure overload has been shown to induce mitogen activated protein kinases (MAPKs) and reactivate ...
Cardiac hypertrophy is an important risk factor for cardiac morbidity and mortality. To unravel the ...
Reversible protein phosphorylation is a posttranslational modification of regulatory proteins involv...
Abstract Cardiac hypertrophy provides an adaptive mechanism to maintain cardiac output in response t...
In response to chronic hypertension, the heart compensates by hypertrophic growth, which frequently ...
To study the role of early energetic abnormalities in the subsequent development of heart failure, w...