Department of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka Street 6/8, Lodz 92-215, Poland; Department of Immunology, Institute of Medical Biotechnology, Tbilisi State Medical University, Chiaureli Street 2a, Tbilisi 0159, Georgia.
Department of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka Street 6/8, Lodz 92-215, Poland.
Ageing Res Rev. 2016 Aug;29:13-25. doi: 10.1016/j.arr.2016.05.011. Epub 2016 May 26.
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.
最近的研究表明,衰老内皮细胞的积累可能是心血管疾病的主要原因。由于内皮细胞具有多功能特性,它们积极参与刺激免疫系统和炎症反应。此外,衰老的特征是免疫细胞的逐渐恶化和免疫反应的激活下降。这导致免疫系统的主要功能丧失,无法消除受损/衰老细胞和中和潜在的有害炎症反应源。在这篇综述中,我们讨论了内皮细胞的细胞衰老和衰老相关分泌表型(SASP),并总结了内皮细胞与免疫衰老之间的联系。我们描述了年龄相关的 Toll 样受体(TLRs)和 microRNAs 的变化如何通过负反馈回路影响衰老内皮细胞和免疫细胞的表型,该负反馈回路旨在抑制过度的促炎反应。这篇综述还探讨了以下问题:衰老的内皮细胞如何影响炎症负担的衰老或与年龄相关的变化;ECs 与免疫衰老之间有什么联系,以及在衰老过程中连接内皮细胞和免疫系统的关键假设途径是什么。