The roles of MTOR and miRNAs in endothelial cell senescence

Area of Science:

• Cardiovascular Biology
• Cellular Senescence
• Molecular Regulation

Background:

• Cellular senescence in vascular endothelium drives vascular aging and cardiovascular disease risk.
• Classical senescence pathways (p53/p21, p16/pRB) are known, but the mammalian target of rapamycin (MTOR) pathway's role is emerging.
• MicroRNAs (miRNAs) are key regulators of gene expression involved in cellular processes, including senescence.

Purpose of the Study:

• To review the roles of MTOR and MTOR-associated miRNAs in endothelial cell senescence.
• To elucidate the crosstalk between MTOR Complex 1 (MTORC1) and cell cycle pathways.
• To discuss the emerging role of MTOR Complex 2 (MTORC2) in cellular senescence.

Main Methods:

• Literature review of studies on MTOR, miRNAs, and endothelial cell senescence.
• Analysis of molecular mechanisms linking MTOR signaling to senescence pathways.
• Examination of the interplay between MTORC1, MTORC2, and cell cycle regulation in senescence.

Main Results:

• MTOR inhibition is linked to blunted senescence and extended lifespan in model organisms.
• Emerging evidence highlights MTOR as a driver of senescence, interacting with classical pathways.
• miRNAs play a crucial role in modulating MTOR activity and endothelial cell senescence.

Conclusions:

• MTOR and miRNAs are critical regulators of endothelial cell senescence.
• Understanding the coordination between MTOR and miRNAs provides deeper insights into vascular aging.
• Further research into these molecular mechanisms can clarify the complexity of cellular senescence regulation.