SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg
This study showed that SENP3 mediated deSUMOylation of CCL17, increase CCL17 expression in macrophage. CCL17 secreted by macrophage regulating Treg recruitment through the competitive interaction between CCL17 and CCL22 and thus aggravated AS. Our findings provide a new regulatory mechanism and potential target for AS treatment.
Authors
- Yicong Ye (ORCID: https://orcid.org/0000-0002-9433-6140)
- Yaodong Ding (ORCID: https://orcid.org/0000-0002-5388-2321)
- Fenfang Zhang
- Xiliang Zhao (ORCID: https://orcid.org/0000-0001-5290-7155)
- Yang Zhang (ORCID: https://orcid.org/0000-0003-3260-1591)
- Jianjun Du (ORCID: https://orcid.org/0000-0002-6572-2720)
- Yong Zeng (ORCID: https://orcid.org/0000-0001-8584-7224)
Institutions
- The People's Hospital Tongling (CN)
- Beijing Anzhen Hospital (CN)
- People's Hospital of Yangzhong (CN)
Publication Details
- Journal
- Cell Biology and Toxicology
- Published
- 2025-11-21
- DOI
- https://doi.org/10.1007/s10565-025-10099-3
- Primary Topic
- Ubiquitin and proteasome pathways
- Type
- article
- Field-Weighted Citation Impact
- 0.00