The Renin-Angiotensin-Aldosterone System as a Therapeutic Target in Late Injury Caused by Ischemia-Reperfusion

Figures

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  Figure 1. Angiotensin and renin genes.

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  Figure 2. Angiotensinogen cleavage. On the left, the normal process of activation of the RAAS. On the right, the RAAS during I/R; the yellow stars signify blockage of the enzyme and diminished expression.

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  Figure 3. Aldosterone synthesis. The process starts with the activation of the AT1R; the G protein is uncoupled and segmented in two fragments. The subunit alpha will activate the phospholipase C which will be produced from PIP2, DAG, and IP3; the DAG will activate the PKC, and then this will phosphorylate the P450 complex, the hormone-sensitive lipase, and the StAR family of cholesterol transporters, which will lead to the production of aldosterone.

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  Figure 4. Dimerization and coupling of receptors.

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  Figure 5. AT1R signaling. The activity of the receptor will stimulate oxidative stress and activation of other signaling pathways.

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  Figure 6. The mineralocorticoid receptor and the epithelial-mesenchymal transition activation.

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  Figure 7. The activation of prorenin receptor during I/R.

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  Figure 8. Formation of oxidative stress in mitochondria by I/R.