ClinicalTrials.gov
public full text
Public Domain
Autophagy Maintains Vascular Function Through a Novel Glycolysis-linked Pathway Regulating eNOS
Aging is inevitable and is the primary risk factor for developing cardiovascular disease. The molecular mechanisms that drive vascular dysfunction in the context of aging are incompletely understood. The overall hypothesis is that the age-related decline in endothelial cell (EC) autophagy leads to arterial dysfunction. This study will determine whether physiological shear-stress affects autophagosome formation and nitrous oxide (NO) generation in ECs.
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- ATG7 vs. ATG5: Distinct autophagy pathways shaping TGF-β signaling and endothelial function#146543
- Autophagy and Venous Endothelial Function#1140057
- Effect of Allopurinol on Mono and Co-administration With Statins on Platelets Reactivity on Diabetic Patiets Treated With Aspirin and Insulin#1032443
- Biomarkers in Vascular Ehlers-Danlos Syndrome#1171042
- Exercise, Arterial Modulation and Nutrition in Youth South Africa Study#900666
Record · ID 863285
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive