Vascular aging integrates cardiometabolic stress into persistent molecular, cellular, and structural injury, yet its variable reversibility remains poorly explained. We propose a vascular memory framework in which prior stress is stored across epigenetic, immune, mitochondrial-redox, senescent, and matrix substrates and recalled as vascular dysfunction. Their differing erasability may guide provisional endotyping and therapeutic selection, distinguish modifiable from persistent injury, and emphasize earlier, substrate-matched intervention before consolidation limits reversibility.
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Sivakumar et al. (2026) studied this question.
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