|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|1902142||1534304||2016||13 صفحه PDF||سفارش دهید||دانلود رایگان|
• Vasculature senescence plays an active role in promoting an inflammatory response.
• Endothelial cells are important contributors to chronic low-grade inflammation.
• Ageing compromises the elimination of senescent cells by the immune system.
• SASP factors promote the development of a senescence phenotype in normal cells.
• The full recovery of immune homeostasis may be controlled with ECs.
Recent studies have demonstrated that the accumulation of senescent endothelial cells may be the primary cause of cardiovascular diseases. Because of their multifunctional properties, endothelial cells actively take part in stimulating the immune system and inflammation. In addition, ageing is characterized by the progressive deterioration of immune cells and a decline in the activation of the immune response. This results in a loss of the primary function of the immune system, which is eliminating damaged/senescent cells and neutralizing potential sources of harmful inflammatory reactions.In this review, we discuss cellular senescence and the senescence-associated secretory phenotype (SASP) of endothelial cells and summarize the link between endothelial cells and immunosenescence. We describe the possibility that age-related changes in Toll-like receptors (TLRs) and microRNAs can affect the phenotypes of senescent endothelial cells and immune cells via a negative feedback loop aimed at restraining the excessive pro-inflammatory response. This review also addresses the following questions: how do senescent endothelial cells influence ageing or age-related changes in the inflammatory burden; what is the connection between ECs and immunosenescence, and what are the crucial hypothetical pathways linking endothelial cells and the immune system during ageing.
Journal: Ageing Research Reviews - Volume 29, August 2016, Pages 13–25