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Updated: Feb 4, 2026

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Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
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Ginsenoside Rb1 Targets the HRD1-STING Axis to Mitigate Cholesterol-Induced VSMC Senescence
Haiming Niu1, Yingzhang Cai2, Conghui Yu2
1Department of Critical Care Medicine, Zhongshan People's Hospital, Zhongshan, People's Republic of China.
Journal of Clinical Laboratory Analysis
|February 2, 2026
Summary
Ginsenoside Rb1 protects vascular smooth muscle cells from cholesterol-induced senescence by preserving HRD1 expression and mitigating ER stress. This suggests Rb1 may prevent vascular diseases linked to VSMC senescence.
Area of Science:
- Cardiovascular Biology
- Cellular Senescence
- Pharmacology
Background:
- Vascular smooth muscle cells (VSMCs) are key to vascular health.
- HRD1 is a potential target for VSMC senescence.
- Ginsenoside Rb1 counters endothelial cell senescence.
Purpose of the Study:
- Investigate Rb1's protective effects on VSMCs against cholesterol-induced senescence.
- Evaluate Rb1's impact on senescence markers, ROS, and STING pathway.
Main Methods:
- VSMCs were pretreated with Rb1 then exposed to cholesterol.
- Assessed SA-β-gal activity, ROS generation, cell viability, and STING activation.
- Utilized HRD1 knockdown and STING inhibitor for mechanistic insights.
Main Results:
- Rb1 reduced cholesterol-induced SA-β-gal-positive cells.
- Rb1 suppressed ER stress markers and STING signaling.
- Rb1 preserved HRD1 expression, reducing ROS and maintaining mitochondrial function.
Conclusions:
- Rb1 protects VSMCs from cholesterol-induced senescence via HRD1 and STING pathways.
- Rb1 mitigates ER stress and preserves mitochondrial function.
- Rb1 shows therapeutic potential for vascular diseases linked to VSMC senescence.
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