ACKR1 <sup>hi</sup> ECs Promote Aortic Dissection Through Adjusting Macrophage Behavior
This study reveals how endothelial cells exhibiting high ACKR1 expression modulate macrophage migration and proinflammatory polarization through the ACKR1/NF-κB/SPP1 signaling pathway, a crucial mechanism in TAAD progression. Targeting ACKR1 through both functional and pharmacological approaches effectively suppressed TAAD progression and extended survival in TAAD mice, offering promising new intervention strategies for clinical evaluation.
Authors
- Jun Ren (ORCID: https://orcid.org/0000-0002-0275-0783)
- Chang Zou (ORCID: https://orcid.org/0000-0002-2003-7834)
- Yazhe Zhou
- Jinquan Xia (ORCID: https://orcid.org/0000-0001-8234-818X)
- Xiangbao Li
- Qijun Zheng (ORCID: https://orcid.org/0000-0002-4525-8537)
- Yayu Wang
- Bin Zhang (ORCID: https://orcid.org/0000-0002-9264-8554)
- Xiong Jia (ORCID: https://orcid.org/0000-0003-3604-7655)
- Yifei Zhang (ORCID: https://orcid.org/0009-0001-7684-3608)
- Xue Yi Zhu
Institutions
- Guangzhou University of Chinese Medicine (CN)
- Ministry of Education of the People's Republic of China (CN)
- Jinan University (CN)
- Guangdong Medical College (CN)
- Fudan University (CN)
- Southern University of Science and Technology (CN)
- Northwest University (CN)
- Chinese University of Hong Kong, Shenzhen (CN)
- Zhongshan Hospital (CN)
- Southern Medical University Shenzhen Hospital (CN)
- Shanghai Clinical Research Center (CN)
Publication Details
- Journal
- Circulation Research
- Published
- 2024-12-18
- DOI
- https://doi.org/10.1161/circresaha.124.325458
- Citations
- 15
- Primary Topic
- Aortic aneurysm repair treatments
- Type
- article
- Field-Weighted Citation Impact
- 6.28