Angiotensin II-Induced Signal Transduction Mechanisms for Cardiac Hypertrophy

Figures

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  Figure 1. A schematic representation for the involvement of different angiotensin peptides such as Ang II and Ang (1-7) as well as their receptors for the development of cardiac hypertrophy upon the activation of renin-angiotensin system. It is pointed out that although other angiotensin peptides such as Ang III, Ang IV and Ang (1-9) are also formed during the activation of renin-angiotensin system, their role and receptor mechanisms are not fully understood.

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  Figure 2. A schematic representation for the AT1 receptors and phospholipase C mediated signal transduction pathways for the development of Angiotensin II- induced cardiac hypertrophy. The activation of AT1R has been shown to promote Ca2+—entry through sarcolemmal Ca2+ channels and increase the intercellular concentration Ca2+, which may also contribute to activating Ca2+ calmodulin kinase for the occurrence of cardiac hypertrophy.

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  Figure 3. A schematic representation for the AT1 receptors and redox status mediated signal transduction pathway as well as AT1 receptor and oxidative stress-calcineurin pathway for the development of acute and chronic cardiac hypertrophy, respectively. Although different other signal transduction pathways such as ROS, PKC, ERK1/2, Akt, NF-κB and NOX, p38 MAPK, c-JNK, NF-κB have been identified to explain Ang II—induced pathological (maladaptive) cardiac hypertrophy, their involvement including that of Ca2+, calmodulin in the development of physiological (adaptive) cardiac hypertrophy is poorly understood.