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Implicating endothelial cell senescence to dysfunction in the ageing and diseased brain
Sara I Graves1, Darren J Baker1,2
1Departments of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.
Basic & Clinical Pharmacology & Toxicology
|March 13, 2020
Summary
Cerebrovascular endothelial cells (CECs) dysfunction, linked to aging and disease, may stem from cellular senescence. This process impacts the blood-brain barrier and neurovascular coupling, contributing to brain health decline.
Area of Science:
- Neuroscience
- Cell Biology
- Vascular Biology
Background:
- Cerebrovascular endothelial cells (CECs) form the blood-brain barrier (BBB) and are crucial for neurovascular coupling.
- CEC dysfunction contributes to aging and cerebrovascular diseases, causing BBB permeability and impaired cerebral blood flow regulation.
- Cellular senescence, a state of irreversible growth arrest with a pro-inflammatory secretory phenotype, is implicated in CEC dysfunction.
Purpose of the Study:
- To review the molecular mechanisms of CEC dysfunction.
- To explore the link between CEC dysfunction and cellular senescence.
- To discuss the role of CEC senescence in age-related cerebrovascular dysfunction.
Main Methods:
- Literature review and synthesis of existing research on CECs, BBB, NVU, and cellular senescence.
- Analysis of molecular changes associated with CEC dysfunction.
- Examination of evidence linking endothelial cell senescence to aging and cardiovascular disease.
Main Results:
- CEC dysfunction shares molecular characteristics with senescent cells.
- Evidence suggests endothelial cell senescence occurs in aging and cardiovascular disease.
- CEC senescence is a potential contributor to age-related cerebrovascular dysfunction.
Conclusions:
- CEC dysfunction in aging and disease may involve cellular senescence.
- Understanding CEC senescence is key to addressing age-related cerebrovascular decline.
- Further research into CEC senescence could reveal therapeutic targets for cerebrovascular disorders.
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