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Updated: Jul 11, 2025

Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood
Published on: September 14, 2017
Marine Compound Exerts Antiaging Effect in Human Endothelial Progenitor Cells via Increasing Sirtuin1 Expression
Jing Yang1, Jie Li2, Ting-Ting Wei1
1Department of Pharmacology, Cardiac & Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China.
Compound 3 (C3) prevents aging in human endothelial progenitor cells (hEPCs) by boosting sirtuin type 1 (SIRT1) and balancing AMPK/Akt pathways. This marine compound shows potential for treating age-related cardiovascular diseases.
Area of Science:
- Cardiovascular Disease Research
- Cellular Aging Mechanisms
- Marine Natural Products
Background:
- Aging increases cardiovascular disease risk.
- Endothelial progenitor cells (hEPCs) are crucial for vascular health.
- Marine-derived compounds are explored for therapeutic potential.
Purpose of the Study:
- To investigate the effects of compound 3 (C3) on senescence in human endothelial progenitor cells (hEPCs).
- To elucidate the molecular mechanisms underlying C3's protective effects against age-related endothelial dysfunction.
Main Methods:
- Induction of hEPC senescence using angiotensin II (AngII).
- Assessment of senescence markers (SA-β-galactosidase, telomerase activity, viability).
- Analysis of key signaling pathways (SIRT1, AMPK, Akt) and intervention with specific inhibitors.
Main Results:
- AngII induced hEPC senescence, decreasing telomerase activity and viability.
- C3 dose-dependently reversed AngII-induced senescence and restored cell function.
- C3 increased SIRT1 expression and modulated AMPK/Akt phosphorylation, effects dependent on SIRT1 activity.
Conclusions:
- Compound 3 protects hEPCs from AngII-induced senescence via SIRT1 upregulation and AMPK/Akt pathway regulation.
- C3 demonstrates potential as a therapeutic agent for aging-related cardiovascular disorders.
- Targeting hEPC senescence with C3 may mitigate endothelial dysfunction in the elderly.
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