Deficiency of ATF3 facilitates both angiotensin II‐induced and spontaneously formed aortic aneurysm and dissection development by activating cGAS–STING pathway
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.
Authors
- Yifan Du (ORCID: https://orcid.org/0000-0002-0734-9200)
- Lingyun Ren
- Manhua Chen (ORCID: https://orcid.org/0000-0003-2118-8818)
- Jiahong Xia (ORCID: https://orcid.org/0000-0003-2144-7525)
- Jingjing Luo (ORCID: https://orcid.org/0000-0003-1298-0803)
- Xiangchao Ding (ORCID: https://orcid.org/0000-0001-6832-9804)
- Ping Ye (ORCID: https://orcid.org/0000-0002-5591-6812)
- Dashuai Wang (ORCID: https://orcid.org/0000-0003-2575-1524)
- Sheng Le
- Poyi Hu
Institutions
- Wuhan University (CN)
- Zhongnan Hospital of Wuhan University (CN)
- Wuhan Union Hospital (CN)
- Renmin Hospital of Wuhan University (CN)
- Central Hospital of Wuhan (CN)
- First Affiliated Hospital of Zhengzhou University (CN)
- Huazhong University of Science and Technology (CN)
Publication Details
- Journal
- Clinical and Translational Medicine
- Published
- 2024-12-27
- DOI
- https://doi.org/10.1002/ctm2.70147
- Citations
- 6
- Primary Topic
- interferon and immune responses
- Type
- article
- Field-Weighted Citation Impact
- 1.44
Funders
- National Natural Science Foundation of China