By what mechanism does elevated homocysteine level cause endothelial dysfunction and damage?
In addition Alan Boyd's answer homocysteine interferes with Glutathione synthesis by reducing the catalytic efficiency of GCL (Glutamate–cysteine ligase), the enzyme which performs the rate-limiting step in GSH synthesis.


  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267299/
  
  Results of the present study are the first to suggest that the relatively high levels of homocysteine that accumulate during aging can interfere with de novo GSH synthesis. Although the precise nature of the underlying mechanism is at present unclear, our results demonstrate that physiological concentrations of free homocysteine can inhibit the efficiency of cysteine utilization by GCL in a competitive manner. Homocysteine has been shown to bind GCLc at the active site in vitro [25] as well as in vivo [35], forming γ-glutamylhomocysteine [36], which is then rapidly degraded enzymatically. An additional mechanism by which an age-related increase in free homocysteine can inhibit the catalytic efficiency of GCL in a competitive manner is described in [35]. It is possible that an aging-related increase in the competition between cysteine and homocysteine for the cysteine binding site of GCL might lead to a decrease in GC synthesis.


Low glutathione means a reduced ability to detoxify and deal with oxidative stress and a more oxidised redox state which has many implications

Further reading:

Inhibition of glutathione synthesis in brain endothelial cells lengthens S-phase transit time in the cell cycle: Implications for proliferation in recovery from oxidative stress and endothelial cell damage
http://www.sciencedirect.com/science/article/pii/S2213231713000244

Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability
http://content.onlinejacc.org/article.aspx?articleid=1125915