Both excessive and insufficient angiogenesis are associated with progression of diabetic complications, of which poor angiogenesis is an important feature. Currently, adipose‐derived stem cells (ADSCs) are considered to be a promising source to aid therapeutic neovascularization. However, functionality of these cells is impaired by diabetes which can result from a defect in hypoxia‐inducible factor‐1 (HIF‐1), a key mediator involved in neovascularization. In the current study, we sought to explore effectiveness of pharmacological priming with deferoxamine (DFO) as a hypoxia mimetic agent, to restore the compromised angiogenic pathway, with the aid of ADSCs derived from streptozotocin (STZ)‐induced type 1 diabetic rats (‘diabetic ADSCs’).

Diabetic ADSCs were treated with DFO and compared to normal and non‐treated diabetic ADSCs for expression of HIF‐1α, VEGF, FGF …

Both excessive and insufficient angiogenesis are associated with progression of diabetic complications, of which poor angiogenesis is an important feature. Currently, adipose‐derived stem cells (ADSCs) are considered to be a promising source to aid therapeutic neovascularization. However, functionality of these cells is impaired by diabetes which can result from a defect in hypoxia‐inducible factor‐1 (HIF‐1), a key mediator involved in neovascularization. In the current study, we sought to explore effectiveness of pharmacological priming with deferoxamine (DFO) as a hypoxia mimetic agent, to restore the compromised angiogenic pathway, with the aid of ADSCs derived from streptozotocin (STZ)‐induced type 1 diabetic rats (‘diabetic ADSCs’).

Diabetic ADSCs were treated with DFO and compared to normal and non‐treated diabetic ADSCs for expression of HIF‐1α, VEGF, FGF …