Second, our in vitro study has provided the first evidence that Txnip is one of the ultimate culprit factors which mediate hyperglycaemia-aggravated oxidative stress and ischaemic injury, and the hyperglycaemia-increased Txnip expression is, at least in part, due to activation of p38 MAPK and inhibition of Akt. Here, AKT1 is linked to Hyperglycemia.