Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging

Area of Science:

• Gerontology and Vascular Biology
• Cellular Senescence Mechanisms

Background:

• Aging leads to organ decline, with accumulating senescent endothelial cells (ECs) increasing vascular dysfunction risk.
• Senescent ECs contribute to cardiovascular diseases like hypertension, diabetes, atherosclerosis, and neurodegeneration.
• These cells exhibit altered protein expression, morphology, and function, causing vascular impairments such as aortic stiffness and inflammation.

Purpose of the Study:

• To review the molecular drivers of endothelial cell senescence.
• To identify signaling pathways implicated in EC senescence.
• To highlight potential therapeutic targets for age-related vascular diseases.

Main Methods:

• Literature review of molecular players and signaling pathways in EC senescence.
• Analysis of molecules including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR.
• Synthesis of current understanding of EC senescence mechanisms.

Main Results:

• Identified key molecular players and signaling pathways promoting EC senescence.
• Detailed the phenotypic and functional changes in senescent ECs.
• Linked EC senescence to specific vascular impairments and age-related diseases.

Conclusions:

• Endothelial cell senescence is a critical factor in age-related vascular dysfunction.
• Understanding the molecular mechanisms of EC senescence is crucial for therapeutic development.
• Targeting specific pathways offers potential for treating cardiovascular diseases associated with aging.