Pro-inflammatory cytokines mediating senescence of vascular endothelial cells in atherosclerosis.
Dongsheng ShangHanqing LiuZhigang TuPublished in: Fundamental & clinical pharmacology (2023)
Atherosclerosis (AS) is a chronic inflammatory vascular disease, and aging is a major risk factor. Accumulation of senescent vascular endothelial cells (VECs) often leads to chronic inflammation and oxidative stress and induces endothelial dysfunction, contributing to the occurrence and development of AS. Senescent cells can secrete a variety of pro-inflammation cytokines to induce senescence of adjacent cells in a paracrine manner, leading to the transmission of signaling of cellular senescence to neighboring cells and accumulation of senescent cells. Recent studies have demonstrated that several pro-inflammatory cytokines, including IL-17, TNF-α, IFN-γ, can induce senescence of VECs. This review summarizes and focuses on the pro-inflammatory cytokines which often induce the senescence of VECs and the molecular mechanisms of these pro-inflammatory cytokines inducing senescence of VECs. Targeting senescence of VECs induced by pro-inflammatory cytokines may provide a potential and novel strategy for prevention and treatment of AS.
Keyphrases
- endothelial cells
- induced apoptosis
- oxidative stress
- dna damage
- cell cycle arrest
- anti inflammatory
- stress induced
- cardiovascular disease
- high glucose
- endoplasmic reticulum stress
- cell death
- type diabetes
- rheumatoid arthritis
- risk assessment
- immune response
- signaling pathway
- risk factors
- ischemia reperfusion injury
- cancer therapy
- dendritic cells
- climate change