2020
DOI: 10.1038/s41418-020-0537-9
|View full text |Cite
|
Sign up to set email alerts
|

CD9 induces cellular senescence and aggravates atherosclerotic plaque formation

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
22
0

Year Published

2020
2020
2024
2024

Publication Types

Select...
8
1
1

Relationship

0
10

Authors

Journals

citations
Cited by 52 publications
(29 citation statements)
references
References 65 publications
1
22
0
Order By: Relevance
“…The significant lower levels of CD9 reported in MD-ASC has never been reported in the literature as a feature of lipomas. Although considered a stem cell marker, it has been recently shown that downregulation of CD9 expression can protect from cellular senescence [40]. CD9 was shown to act through a phosphatidylinositide 3 kinase-AKT-mTOR-p53 signal pathway and it would be interesting in the future to investigate this pathway in MD-ASC.…”
Section: Discussionmentioning
confidence: 99%
“…The significant lower levels of CD9 reported in MD-ASC has never been reported in the literature as a feature of lipomas. Although considered a stem cell marker, it has been recently shown that downregulation of CD9 expression can protect from cellular senescence [40]. CD9 was shown to act through a phosphatidylinositide 3 kinase-AKT-mTOR-p53 signal pathway and it would be interesting in the future to investigate this pathway in MD-ASC.…”
Section: Discussionmentioning
confidence: 99%
“…Such changes cause accumulation of LDL in the sub-endothelial space resulting in enhanced EC expression of adhesion molecules such as vascular cell adhesion molecule 1 (VCAM1), E- and P-Selectins to promote leukocyte recruitment ( 73 ). CD9, a novel senescence-related marker was reported to be increased in aged human arteries and mice ( 74 ). In mouse models of atherosclerosis, CD9 expression was co-expressed with SA-β-gal staining and was found the be upregulated in ECs and macrophages within lesions.…”
Section: Endothelial Cell Senescence In Age-related Diseasesmentioning
confidence: 99%
“…For example, tetraspanin 8 interacted with rictor, a key component of mTOR complex 2 (mTORC2) in malignant glioma (22). CD9 (TSPAN29) induced senescence in human endothelial cells via regulating PI3K/AKT-mTOR pathway (23). It is also reported that CD82 overexpression in multiple myeloma cell lines resulted in upregulation of phospho-S6 ribosomal protein, an established target of mTORC1 (24).…”
Section: Read Full Licensementioning
confidence: 99%