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. 2014 Nov 11;5:242. doi: 10.3389/fphar.2014.00242

FIGURE 7.

FIGURE 7

Schematic of proposed EET cardioprotective mechanism(s). LPS triggers activation of NF-κB-dependent signaling and suppresses PPARγ activation, resulting in a shift of the cellular response to a pro-inflammatory state. Increased EETs can act as PPARγ agonists and inhibit NF-κB-dependent signaling, shifting the cellular response to an anti-inflammatory state.