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. 2020 May 14;32(18):1293–1312. doi: 10.1089/ars.2019.7808

FIG. 8.

FIG. 8.

Correlation between redox status and functional changes indicated a cRS condition induces pathologic cardiac remodeling. Correlations among redox status (dose and time dependent) and cardiac functional outcomes (systolic and diastolic) are demonstrated in both young (2, 3, and 6 months) and old (15 months) TGL, TGH, and DTG mice, indicating remarkable impacts of cRS on both (A) systolic (i.e., EF%) and (B) diastolic (i.e., M/V E/A ratio) functions. (C) The diastolic function was deteriorating to increase reductive potential, whereas systolic function was elevated, suggesting that (D) varying degrees of reductive-redox through dose- and time-dependent Nrf2 expression influence on the structural and functional phenotypes of heart. (E) A schematic overview of how the caNrf2 expression induces cRS and depletes biological ROS signals, as well as how cRS (>6 months) induces the cardiac structural and functional remodeling by promoting cardiac hypertrophy and diastolic dysfunction. Doubling the myocardial Nrf2 levels (in DTG) further advances RS and accelerates cardiac remodeling/diastolic dysfunction as early as 1.8 months of age. Pharmacologic depletion of glutathione using BSO abolishes RS-mediated myocardial remodeling. cRS, chronic reductive stress; ROS, reactive oxygen species. Color images are available online.