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Pressure overload (PO) and volume overload (VO) lead to concentric or eccentric hypertrophy. Previously, we could show that activation of signalling cascades differ in in vivo mouse models. Activation of these signal cascades could either be induced by intrinsic load sensing or neuro-endocrine substances like catecholamines or the renin-angiotensin-aldosterone system. We therefore analysed the activation of classical cardiac signal pathways [mitogen-activated protein kinases (MAPKs) (ERK, p38, and JNK) and Akt-GSK3β] in in vitro of mecha
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