As the increased circulatory level of sFlt-1 is associated with cardiovascular complications, such as chronic heart failure [46,47], we sought to investigate whether HO-1 and sFlt-1 play a role in the regulation of cardiac mitochondrial activity using a well-established model of high sFlt-1 environment by the tail-vein injection of adenovirus sFlt-1 in Hmox1+/− mice. The gene discussed is HMOX1; the disease is congestive heart failure.