The functional role of cellular senescence during vascular calcification in chronic kidney disease

Area of Science:

• Cardiovascular Biology
• Nephrology
• Cellular Aging

Background:

• Vascular calcification (VC) is a major risk factor for cardiovascular events in chronic kidney disease (CKD).
• Accelerated vascular aging and cellular senescence are increasingly recognized as key contributors to VC in CKD.
• Senescent vascular cells release factors that promote calcification and inflammation.

Purpose of the Study:

• To comprehensively review the role of vascular cell senescence in the development and progression of VC.
• To highlight the mechanisms by which cellular senescence contributes to VC in CKD patients.
• To underscore the importance of understanding cellular senescence for developing anti-aging therapies for cardiovascular disease.

Main Methods:

• Literature review of studies investigating vascular cell senescence and VC in CKD.
• Analysis of mechanisms involving senescent vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs).
• Examination of the senescence-associated secretory phenotype (SASP) and its inflammatory effects.

Main Results:

• Senescent VECs release microvesicles that induce VSMC senescence and osteogenic transition, promoting VC.
• Senescent vascular progenitor cells have impaired differentiation and release SASP, perpetuating senescence.
• SASP creates a pro-inflammatory microenvironment, recruiting immune cells and exacerbating VC.

Conclusions:

• Vascular cell senescence is a critical driver of VC in CKD, contributing to accelerated vascular aging.
• Targeting cellular senescence and SASP may offer novel therapeutic strategies for mitigating cardiovascular disease in CKD.
• Understanding the interplay between senescence and VC is crucial for advancing anti-aging interventions.