Deficiency of ATF3 facilitates both angiotensin II-induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS–STING pathway

Yifan Du , Poyi Hu , Xiangchao Ding , Dashuai Wang , Jingjing Luo , Sheng Le , Lingyun Ren , Manhua Chen , Ping Ye , Jiahong Xia

Clinical and Translational Medicine ›› 2025, Vol. 15 ›› Issue (1) : e70147

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Clinical and Translational Medicine ›› 2025, Vol. 15 ›› Issue (1) : e70147 DOI: 10.1002/ctm2.70147
RESEARCH ARTICLE

Deficiency of ATF3 facilitates both angiotensin II-induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS–STING pathway

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Abstract

•ATF3 deficiency led to degradation of P21 through ubiquitination, which abolished the G1 phase arrest.

•VSMCs had no time window to repair the damaged DNA, leading to generation of micronuclei in cytoplasm.

•Cytoplasmic micronuclei facilitating the activation of cGAS–STING pathway, thus inducing the phenotypic switch and apoptosis of VSMCs

Keywords

aortic aneurysm and dissection / cGAS–STING pathway / DNA stability / micronuclei formation / P21

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Yifan Du, Poyi Hu, Xiangchao Ding, Dashuai Wang, Jingjing Luo, Sheng Le, Lingyun Ren, Manhua Chen, Ping Ye, Jiahong Xia. Deficiency of ATF3 facilitates both angiotensin II-induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS–STING pathway. Clinical and Translational Medicine, 2025, 15(1): e70147 DOI:10.1002/ctm2.70147

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2024 The Author(s). Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics.

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