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. 2023 Jan 4;55(1):1–12. doi: 10.1038/s12276-022-00906-w

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Endothelial senescence is characterized by an age-associated decline in endothelial function, which includes the loss of control over vasodilation, blood coagulation, oxidative stress, inflammation, immune cell infiltration, and glucose and lipid dynamics mediated by endothelium-derived factors, such as nitric oxide (NO), endothelin-1 (ET-1), prostaglandin (PG), thromboxane (TX), endothelial growth factor (EGF) and angiotensin-converting enzyme (ACE). A reduction in NO, the master regulator of the endothelium, is one of the primary factors driving these changes. Other factors include increased reactive oxygen species (ROS) levels and senescence-associated secretory phenotype (SASP) acquisition. EC endothelial cell, eNOS endothelial nitric oxide synthase.