Role of Oxidative Stress in Thyroid Hormone-Induced Cardiomyocyte Hypertrophy and Associated Cardiac Dysfunction: An Undisclosed Story

Figure 3

Molecular changes in the hyperthyroid hearts in response to increased oxidative stress. This includes main (1) antioxidant, (2) hypertrophic, and (3) apoptotic signaling activated by oxidative stress in. T4: thyroxin; T3: triiodothyronine; Nrf-2: NF-E2-related factor 2; Trx: thioredoxin; Prx: peroxiredoxin; IGF-IR: insulin growth factor-I receptors; AKT-1 (PKB): protein kinase B; ERK: extracellular regulated kinase; WT: wild-type; THs: thyroid hormones; Bax: Bcl-2: Bcl-2 family proteins where Bax is proapoptotic while Bcl-2 is antiapoptotic; +: activation; ?: not shown in this study. Representative image of thyroid gland is copied from Wikipedia under the Creative Commons Attribution-Share Alike 3.0 Unported License, which allows sharing and/or remixing. Images of cardiomyocytes from wild-type (WT) and thyroid hormone- (TH-) treated mouse hearts are adapted from Elnakish et al. 2012 [16].