NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy

• Published in: Scientific reports Vol. 14; no. 1; pp. 6971 - 14
• Main Authors: Ma, Yuan, Zhao, Hui-Ping, Yang, Li-Guo, Li, Lu, Wang, Ai-Lin, Zhang, Xiao-Juan, Wang, Ke, Yang, Bin, Zhu, Zong-Feng, Zhang, Pei-Jun, Wang, Jia-Pu, Chi, Rui-Fang, Li, Bao, Qin, Fu-Zhong, Wang, Zhi-Peng
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 23.03.2024; Nature Publishing Group; Nature Portfolio
• Subjects: 631/443/592/75/230; 631/443/592/75/74; Animals; Antineoplastic drugs; Atrophy; Autophagy; Cardiomyopathies - chemically induced; Cardiomyopathies - metabolism; Cardiomyopathy; Cardiotoxicity; Congestive heart failure; CYBB protein; Denervation; Doxorubicin; Doxorubicin - pharmacology; Heart diseases; Humanities and Social Sciences; Mice; Mice, Inbred C57BL; Mice, Knockout; multidisciplinary; Myocytes; Myocytes, Cardiac - metabolism; NAD(P)H oxidase; NADPH Oxidase 2 - genetics; NADPH Oxidase 2 - metabolism; NADPH Oxidase 4 - metabolism; Norepinephrine; Norepinephrine transporter; Oxidative Stress; Science; Science (multidisciplinary); Survival; Sympathectomy; Sympathetic nerves; Tyrosine 3-monooxygenase

Doxorubicin has been used extensively as a potent anticancer agent, but its clinical use is limited by its cardiotoxicity. However, the underlying mechanisms remain to be fully elucidated. In this study, we tested whether NADPH oxidase 2 (Nox2) mediates cardiac sympathetic nerve terminal abnormaliti...