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. 2020 Oct 19;78(4):1329–1354. doi: 10.1007/s00018-020-03664-y

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Consequences of ERK and p21 activation in aged blood vessels. In quiescent vessels of young individuals, p21 expression and transient ERK activation occur only sporadically in ECs as quiescence is maintained independently of p21. With progressing age, p21-positive cells having ERK constitutively activated accumulate in blood vessels. This senescent phenotype promotes a pro-inflammatory and pro-thrombotic environment in the endothelium, impairs vasodilation, and leads to dysfunctional angiogenesis