In summary, these findings demonstrate that the overexpression of Adra2a can reduce the secretion of growth factors in ASCs, and knocking down Adra2a in T2D ASCs can restore the ability of T2D ASCs to secrete growth factors, which provides a possibility to shrink the difference of normal and T2D ASCs in clinical studies. Here, ADRA2A is linked to type 2 diabetes mellitus.