Key result
In mice, direct AngII activates p38 while mechanical stress stimulates ERK and JNK.
Why the study?
The study aimed to determine whether AngII-induced cardiac hypertrophy and haemodynamic load are associated with specific cardiac MAPK pathway activation during hypertrophy development.
Population
Normotensive and hypertensive transgenic mice with AngII-mediated cardiac hypertrophy and physiological models of renovascular hypertension
Comparison
AngII-dependent vs AngII-independent renovascular hypertension models; normotensive vs hypertensive mice
Design
Preclinical experimental study
Authors
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Distinguishes direct AngII effects from mechanical stress on cardiac MAPK pathways in mice; leaves open translation to human hypertension or HF therapies.
In mouse models of cardiac hypertrophy, p38 activation is linked to direct AngII effects, while ERK and JNK activation is driven by mechanical stress.
Pellieux et al. (2000) studied Cardiac hypertrophy. Angiotensin II (AngII) and haemodynamic load vs. AngII-independent and normotensive models was evaluated on Activation of cardiac MAPK pathways (ERK, JNK, p38). In mice, p38 activation is preferentially associated with the direct effects of AngII on cardiac cells, whereas stimulation of ERK and JNK occurs in association with AngII-induced mechanical stress.
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