Bach1 is a known transcriptional repressor of the heme oxygenase-1 (HO-1) gene. 
The purpose of this study was to determine whether angiogenesis is accelerated 
by genetic ablation of Bach1 in a mouse ischemic hindlimb model. Hindlimb 
ischemia was surgically induced in wild-type (WT) mice, Bach1-deficient 
(Bach1-/-) mice, apolipoprotein E-deficient (ApoE-/-) mice, and Bach1/ApoE 
double-knockout (Bach1-/-/ApoE-/-) mice. Blood flow recovery after hindlimb 
ischemia showed significant improvement in Bach1-/- mice compared with that in 
WT mice. Bach1-/-/ApoE-/- mice showed significantly improved blood flow recovery 
compared with that in ApoE-/- mice to the level of that in WT mice. Migration of 
endothelial cells in ApoE-/- mice was significantly decreased compared with that 
in WT mice. Migration of endothelial cells significantly increased in 
Bach1-/-/ApoE-/- mice compared with that in ApoE-/- mice to the level of that in 
WT mice. The expression levels of HO-1, peroxisome proliferator-activated 
receptor γ co-activator-1α, angiopoietin 1, and fibroblast growth factor 2 in 
endothelial cells isolated from Bach1-/-/ApoE-/- mice were significantly higher 
than those in ApoE-/- mice. Oxidative stress assessed by anti-acrolein antibody 
staining in ischemic tissues and urinary 8-isoPGF2α excretion were significantly 
increased in ApoE-/- mice compared with those in WT and Bach1-/- mice. Oxidative 
stress was reduced in Bach1-/-/ApoE-/- mice compared with that in ApoE-/- mice. 
These findings suggest that genetic ablation of Bach1 plays an important role in 
ischemia-induced angiogenesis under the condition of increased oxidative stress. 
Bach1 could be a potential therapeutic target to reduce oxidative stress and 
potentially improve angiogenesis for patients with peripheral arterial disease.