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. Author manuscript; available in PMC: 2019 Aug 2.
Published in final edited form as: J Vasc Res. 2018 Aug 2;55(4):210–223. doi: 10.1159/000490244

Figure 1. Age-associated proinflammatory signaling cascades at the molecular, cellular, and tissue levels in the arterial wall.

Figure 1.

The age-associated vascular molecular cascades are triggered by changes due to physical/mental stress allostatic load on the organism. These molecular changes impact the interconnected RAAS and the SNA systems, thus, activating ET-1, and lead to the secretion of downstream molecules and transcription factors.

Abbreviations and acronyms: α-AR: alpha-adrenergic receptor; ACE1/2: angiotensin converting enzyme; AAASP: age-associated arterial secretory phenotype; AGEs: advanced glycoxidation end-products; ALP: alkaline phosphatase; Ang I: angiotensin I; Ang II: angiotensin II; BP: blood pressure; EC: endothelial cells; ECM: extracellular matrix; Ets-1: the v-ets erythroblastosis virus E26 oncogene homolog 1; MCP-1: monocyte chemo-attractant protein-1; MFG-E8: milk fat globule epidermal growth factor-8; MMPs: matrix metalloproteases; MR: mineralocorticoid receptors; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; Nrf2: NF-E2- related factor 2; NO: nitric oxide; PDGF: platelet derived growth factor; PWV: pulse wave velocity; RAGE: receptor for advanced glycoxidation end products; ROS: reactive oxygen species; RS: replicative senescence; SASP: senescence-associated secretory phenotype; Sirt1: silent information regulation 2 homolog 1; SIPS: stress-induced premature senescence; TGF-β1: transforming growth factor β1; SASP: senescence-associated secretory phenotype; VSMC: vascular smooth muscle cell.