Melinda S. Yates

TL;DR: Protection from CS-induced emphysema depended on NRF2, as Nrf2−/− mice failed to show significant reduction inAlveolar cell apoptosis and alveolar destruction after treatment with CDDO-Im, which suggests that targeting the Nrf1 pathway during the etiopathogenesis of emphySEma may represent an important approach for prophylaxis against COPD.

TL;DR: The results suggest that Nrf2 is associated with oxidative regulation of LPS induced innate immune response in neutrophils and Activation of NRF2-dependent compensatory antioxidative pathways by CDDO-Im protects from L PS induced inflammatory response and mortality.

TL;DR: The pharmacodynamic activity of CDDO-Im is characterized in two distinct lines of ARE reporter mice and by measuring increases in Nqo1 transcript levels as a marker of cytoprotective gene induction, highlighting the chemopreventive promise of several synthetic triterpenoids in multiple target organs.

TL;DR: It is indicated that CDDO-Im is an exceedingly potent agent for preventing obesity, and the Nrf2 pathway is identified as a novel target for management of obesogenesis.

TL;DR: Analysis of pharmacologic activation suggests that Nrf2 is the primary mediator of CDDO-Im activity, though other cell-signaling targets are also modulated following an oral dose of 30 micromol/kg.