Figure 8 from Novel Mechanism of and Therapeutic Approach for Anthracycline-Induced Cardiotoxicity

作者：Qingzhu Wang, Wanying Zhang, Josephine Chen, Kate Stenson, Shikha Parsai, Prerana Bangalore Parthasarathy, Chia‐Feng Liu, Thomas Garrett, Jung Lin, Anlin Hou, Riya A. Shimpi, Eric Gu, Mei Yin, Logan Shannon, Sadie Johnson, Belinda Willard, E. Rene Rodriguez, Charlie Androjna, Rohit Moudgil, Yilun Sun, Jennifer S. Yu, Christopher Nguyen, Tyler Alban, Timothy A. Chan, Sathyamangla V Naga Prasad, W.H. Wilson Tang, Jianhong Lin, Jianjun Zhao · 年份：2026 · DOI：10.1158/2767-9764.32730070 · 研究领域：Chemotherapy-induced cardiotoxicity and mitigation、Lung Cancer Research Studies、Chemotherapy-induced organ toxicity mitigation

TOP2B ASO prevents cardiotoxicity in TOP2B transgenic mice and in an AIC mouse model. A, Western blot analysis showing suppression of TOP2B expression following transfection with TOP2B ASO in a cardiomyocyte cell line. B, Dose-dependent Western blot analysis of TOP2B ASO-18 and ASO-19 verifying their effects on TOP2B and TOP2A expression. C, Seahorse XF analysis of mitochondrial OCR in cells transfected with control GFP ASO or TOP2B ASO, with or without doxorubicin treatment. Key mitochondrial parameters measured include basal respiration, ATP-linked respiration, maximal respiration, reserve capacity, proton leak, and nonmitochondrial respiration. Data represent the mean ± SEM. Statistical significance was determined using an unpaired two-tailed Student t test; *, P < 0.05. D, Schematic of the TOP2B transgenic mouse heart failure model used for in vivo testing. E,In vivo experiment showing that TOP2B ASO-18 treatment provides cardioprotective effects compared with dexrazoxane or saline in TOP2B transgenic mice (n = 8 for each group). F, Schematic of the AIC mouse model used for in vivo testing. G,In vivo experiment showing that TOP2B ASO-18 treatment provides cardioprotective effects compared with dexra...