cardiovascular system
N |
• mice exhibit normal basal cardiac function
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• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• increased left ventricle end diastolic/systolic diameter following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• increased collagen content in both the perivascular and interstitial spaces following transaortic constriction
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• following transaortic constriction
• however, treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• lower fractional shortening and ejection fraction following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• following transaortic constriction, mice exhibit increased heart and lung weight, decreased heart function (increased left ventricle end diastolic/systolic diameter, and lower fractional shortening and ejection fraction), and increased collagen content compared with control mice
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
growth/size/body
• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
homeostasis/metabolism
• following transaortic constriction, mice exhibit increased heart and lung weight, decreased heart function (increased left ventricle end diastolic/systolic diameter, and lower fractional shortening and ejection fraction), and increased collagen content compared with control mice
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
muscle
• lower fractional shortening and ejection fraction following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
respiratory system
• following transaortic constriction
• however, infection with an Fbxw5-expressing adenovirus rescues protects mice from cardiac hypertrophy and treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|
cellular
• following transaortic constriction
• however, treatment with iTAK1 5Z-7-oxozeaenol to inhibit TAK1 phosphorylation abolishes the sensitivity to cardiac hypertrophy
|