Toshiya Atsumi

TL;DR: It is shown that macrophage migration inhibitory factor (MIF), an upstream regulator of inflammation, is released in the ischaemic heart, where it stimulates AMPK activation through CD74, promotes glucose uptake and protects the heart during ischaemia-reperfusion injury.

TL;DR: It is reported that the expression of iPFK-2 mRNA and protein, as assessed by in situ hybridization and immunohistochemistry, is increased in many human cancers when compared with corresponding normal tissues and may serve as an essential regulator of glycolysis during cell cycle progression and growth in an hypoxic microenvironment.

TL;DR: Since OPB-9195, an AGE-inhibitor, prevented the progression of diabetic nephropathy by blocking type IV collagen production and suppressing overproduction of two growth factors, TGF-β and VEGF, in diabetic rats, this compound warrants further investigation.

TL;DR: Highly phosphorylated PFKFB3 protein was found in human tumor cells, vascular endothelial cells, and smooth muscle cells, as determined by immunostaining with an anti-phospho-PFK-2(PFK FB3) antibody.

TL;DR: An unexpected role is described for MIF in the regulation of glycolysis, which is associated with the recent finding that MIF is a positive, autocrine stimulator of insulin release, and suggest an important role for Mif in the control of host glucose disposal and carbohydrate metabolism.