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Table 1 Major SASP components in different senescent cell types contribute to the mechanisms of atherosclerosis

From: The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities

Cell type

SASP components

Effect on atherosclerosis

References

Senescent endothelial cell

IL-6

Form atherosclerotic plaques and cause thrombosis

[52]

IL-1

Recruit more immune cells and form atherosclerotic plaques

[95]

IL-8

Form atherosclerotic plaques and cause thrombosis

[52]

IL-15

Form atherosclerotic plaques

[52]

MCP-1

Recruit more immune cells and form atherosclerotic plaques

[95]

TNF

Recruit more immune cells and form atherosclerotic plaques

[95]

ICAM-1,VCAM-1

Recruit circulating monocytes and vascular injury

[17, [96]

ET-1

Vascular endothelial dysfunction

[97]

PAI-1

Cause thrombosis

[95, 98]

VEGF

Promote plaque angiogenesis and vascular remodeling

[99, 100]

Senescent vascular smooth muscle cell

IL-1α

Leading to inflammation and monocyte chemotaxis, and proteolysis

[17]

IL-6

Leading to inflammation and impaired vascular mitochondrial function

[45]

IL-8

Induce angiogenesis in coronary plaques

[101]

CCL-3, 4

Recruit monocyte/macrophage cells and increase plaque size

[101]

MCP-1

Recruit monocyte cells

[17]

TGF-β1

Enhance arterial stiffness and initiate the senescence of other cells

[102]

MMP-1,2,3,7,8,9, 10,12,13,14

Fibrous cap of the plaque becomes thinner and extracellular matrix degradation

[103, 104]

OPG

Vascular calcification;

[105]

VEGF

Promote plaque angiogenesis and vascular remodeling

[99, 100]

Senescent T cell

IL-6

Leading to inflammation

[68]

TNF-α

Leading to inflammation

[68, 106]

IFN-γ

Induces the activation of macrophages

[107]

Senescent macrophage

IL-1β

Leading to inflammation

[11, 108]

IL-6

Leading to inflammation

[11, 108]

TNF-α

Leading to inflammation

[11, 109]

MMP-3, 13

Extracellular matrix degradation and thinning of the fibrous cap in artery

[17, 110]