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Long-term Senolytic Treatment Prevents Endothelial Dysfunction in Arterial Aging
Jie Lin1, Shilin Chen2,3, Dong Tan3
1Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, China.
Abstract:
Endothelial senescence is a critical contributor of arterial dysfunction and age-related cardiovascular diseases. This study demonstrates that long-term senolytic treatment with dasatinib plus quercetin (D+Q; 5 mg/kg + 50 mg/kg biweekly for 8 months) in mice significantly attenuates vascular endothelial senescence. D+Q lowered senescence markers (p21 protein and SA-β-gal positivity) in aged mesenteric arteries and human umbilical vein endothelial cells (HUVECs), while maintaining endothelial integrity. Transcriptomic analysis indicated activation of the relaxin signaling pathway and upregulation of nitric oxide synthase isoforms. Mechanistically, D+Q reversed age-related eNOS uncoupling by promoting dimerization, increased nitric oxide bioavailability, and reduced mitochondrial dysfunction, evidenced by restored mitochondrial ultrastructure, decreased mitochondrial mass, and lowered reactive oxygen species (ROS) production. Consequently, D+Q restored endothelium-dependent vasodilation and enhanced blood flow in aged mesenteric arteries following acetylcholine stimulation. These findings demonstrate that clearance of senescent endothelial cells via senolytic therapy mitigates arterial aging by restoring mitochondrial homeostasis and eNOS function, highlighting its therapeutic potential for age-related vascular dysfunction.
Insights
Senolytic treatment with dasatinib plus quercetin (D+Q) clears senescent endothelial cells, mitigating arterial aging. This therapy restores mitochondrial function and nitric oxide production, improving vascular health in aged mice.
Area of Science:
- Cardiovascular Biology
- Gerontology
- Cellular Senescence
Background:
- Endothelial senescence is a key factor in arterial dysfunction and age-related cardiovascular diseases.
- Senescent cells accumulate with age, contributing to tissue dysfunction and chronic diseases.
Purpose of the Study:
- To investigate the long-term effects of senolytic treatment (dasatinib plus quercetin, D+Q) on vascular endothelial senescence and function in aged mice.
- To elucidate the molecular mechanisms by which D+Q impacts endothelial cells, mitochondrial function, and vascular reactivity.
Main Methods:
- Long-term administration of D+Q (5 mg/kg + 50 mg/kg biweekly for 8 months) to aged mice.
- Assessment of senescence markers (p21, SA-β-gal) in mesenteric arteries and human umbilical vein endothelial cells (HUVECs).
- Transcriptomic analysis, assessment of eNOS (endothelial nitric oxide synthase) coupling and dimerization, mitochondrial function (ultrastructure, mass, ROS production), and vasodilation assays.
Main Results:
- D+Q treatment significantly reduced endothelial senescence markers in aged arteries and HUVECs.
- The therapy restored endothelial integrity, reversed age-related eNOS uncoupling, increased nitric oxide bioavailability, and improved mitochondrial homeostasis (reduced ROS, restored ultrastructure).
- D+Q enhanced endothelium-dependent vasodilation and blood flow in aged mesenteric arteries.
Conclusions:
- Clearance of senescent endothelial cells using D+Q senolytic therapy effectively mitigates arterial aging.
- The therapeutic benefits are linked to restored mitochondrial function and enhanced eNOS activity.
- Senolytic therapy holds significant potential for treating age-related vascular dysfunction.
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