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Editorial
. 2016 Oct;112(1):426-8.
doi: 10.1093/cvr/cvw199.

Conflicting mechanisms of AT2 cardioprotection revealed

Raffaele Altara  1 , Sean P Didion  2 , George W Booz  2
Affiliations
Editorial

Conflicting mechanisms of AT2 cardioprotection revealed

Raffaele Altara et al. Cardiovasc Res. 2016 Oct.
No abstract available

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Figures

Figure 1
Figure 1
Yin and yang of the angiotensin II type 2 (AT2) receptor in cardiovascular protection. Activation of the AT2 receptor has been implicated in protecting the heart from damage and adverse remodeling before or after ischemic assault. Many of the beneficial actions of AT2 in this context are attributed to anti-inflammatory or anti-oxidative mechanisms, involving inhibition or activation of various genes. Protection involves cardiac cells and infiltrating leukocytes or stem/progenitor cells that express AT2 receptors. Recent evidence also links the AT2 receptor to anti-atherogenic effects due to inhibition of endothelial inflammation and leukocyte adhesion. In contrast to these protective, ‘anti’ actions of AT2, Caillon et al. provide evidence in this issue that memory T cells/Th17 cells promote arteriogenesis by producing IL-17 via an AT2-driven process. This finding indicates that the AT2 receptor may also be linked to pro-inflammatory events in protecting the heart. EC, endothelial cells; HF, heart failure; MΦ, macrophages.
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