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. 2017 Jan 16;7:40523. doi: 10.1038/srep40523

Figure 2. LXR-α involved in the feedback loop of AT1R/p38 MAPK-RAS axis and the interventional effect of PFD.

Figure 2

Myocardial injury activated the AT1R/p38 MAPK pathway that disrupted the ACE/ACE2 ratio and further imbalanced ACE-Ang II-AT1R and ACE2-Ang(1-7)-Mas axes, including increases in ACE, Ang II, and AT1R and decreases in ACE2, Ang(1-7) and Mas. Moreover, increasing Ang II and decreasing Ang(1-7) synergistically inhibited LXR-α expression. Consequently, the decrease in LXR-α further activated the AT1R/p38 MAPK pathway. This signalling created a positive feedback loop that amplified AT1R/p38 MAPK signalling, thereby disrupting the RAS balance and inducing cardiac fibrosis. Interestingly, PFD activated LXR-α expression, inhibited the AT1R/p38 MAPK pathway, and balanced the RAS in this rat model of cardiac fibrosis.