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. Author manuscript; available in PMC: 2013 Jul 3.
Published in final edited form as: Cardiovasc Res. 2009 Jul 7;84(1):24–32. doi: 10.1093/cvr/cvp236

Figure 1.

Figure 1

A model for the mechanisms of age-dependent endothelial dysfunction. Physiological levels of stress on the endothelium are generated by heartbeats and metabolic oxidative stress. Upon addition of a risk factor such as hypertension, damage increases, augmenting endothelial cell turnover and thus senescence.25 Exponential accumulation of senescent endothelial cells is pro-atherogenic.

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