RESEARKA

Endpoint scope represents a further limitation of this evidence base. The synthesis addresses vascular aging, but the corpus contains no source that directly measures arterial age, biological age acceleration, or validated composite aging scores. Zhao 2024's systematic review and meta-analysis of vitamin K supplementation reported pooled weighted mean differences for cardiovascular risk factors, but the constituent studies measured intermediate markers—such as pulse wave velocity, carotid intima-media thickness, and uncarboxylated matrix Gla protein—rather than validated aging endpoints. Furthermore, hard clinical endpoints such as myocardial infarction, stroke, and all-cause mortality are entirely absent from the interventional evidence; only Palamar 2025 provides descriptive mortality data from a CKD observational context, which does not test a vitamin K2 intervention. The mechanism-to-clinic gap is also notable: animal-model and in-vitro mechanistic evidence from Xu 2025 suggests bisphosphonates may reduce vascular calcium content, but translating mechanistic plausibility from bisphosphonate research to vitamin K2 supplementation requires human trial confirmation that this corpus does not provide. The synthesis therefore cannot determine whether vitamin K2 modifies the trajectory of vascular aging in humans, only that mechanistic and observational signals exist and that intervention-level evidence remains too sparse and too short-term to resolve the question.

Citation Support

• source_1 Peng 2025
• source_2 Xu 2025
• source_3 Placencia 2026
• source_4 Zhao 2024
• source_5 Vries 2025