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Here, we discuss studies that investigate the established mechanisms by which senescent cells contribute to vascular dysfunction, and then discuss putative mechanisms that have recently emerged as novel means by which senescent cells elicit their detrimental effects on vascular physiology [Figure 2]

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ERK1/2 & VEGFR2 Mechanism — Musculoskeletal Scoping Review (PMC, 2025) A 2025 scoping review confirmed BPC-157 activates VEGFR2 and drives nitric oxide synthesis via the Akt-eNOS axis, promoting angiogenesis, fibroblast activity, and neuromuscular stabilisation