Sensing mitochondrial DNA stress in cardiotoxicity

Yang-Nan Ding; Xiaoqiang Tang

doi:10.1016/j.tem.2023.08.012

Sensing mitochondrial DNA stress in cardiotoxicity

Trends Endocrinol Metab. 2023 Nov;34(11):688-690. doi: 10.1016/j.tem.2023.08.012. Epub 2023 Sep 4.

Authors

Yang-Nan Ding¹, Xiaoqiang Tang²

Affiliations

¹ Department of Laboratory Medicine, Third Affiliated Hospital of Zhengzhou University, 7 Kangfu Qian Street, Zhengzhou, Henan 450052, China.
² Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, No.17 People's South Road, Chengdu, Sichuan 610041, China; National Health Commission Key Laboratory of Chronobiology, Sichuan University, No.17 People's South Road, Chengdu, Sichuan 610041, China; Development and Related Diseases of Women and Children, Key Laboratory of Sichuan Province, West China Second University Hospital, Sichuan University, No. 17 People's South Road, Chengdu, Sichuan 610041, China. Electronic address: tangxiaoqiang@scu.edu.cn.

PMID: 37673764
DOI: 10.1016/j.tem.2023.08.012

Abstract

Cytoplasmic mitochondrial DNA (mtDNA) can trigger the interferon response to promote disease progression, but mtDNA sensing mechanisms remain elusive. Lei et al. have shown that Z-DNA binding protein1 (ZBP1) cooperates with cyclic GMP-AMP synthase (cGAS) to sense Z-form mtDNA and transmit mtDNA stress signals to promote diseases such as cardiotoxicity, providing an important piece of the mtDNA stress landscape.

Keywords: Z-DNA; ZBP1; cGAS; cardiotoxicity; mtDNA.