scispace - formally typeset
T

Takeshi Matsumura

Researcher at University of Tokyo

Publications -  34
Citations -  4877

Takeshi Matsumura is an academic researcher from University of Tokyo. The author has contributed to research in topics: Computer science & Phosphorylation. The author has an hindex of 8, co-authored 21 publications receiving 4663 citations. Previous affiliations of Takeshi Matsumura include Niigata University & Tokyo Denki University.

Papers
More filters

superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This paper showed that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and that this increase in reactive oxygen can be prevented by an inhibitor of electron transport chain complex II, an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
Journal ArticleDOI

Activation of AMP-Activated Protein Kinase Reduces Hyperglycemia-Induced Mitochondrial Reactive Oxygen Species Production and Promotes Mitochondrial Biogenesis in Human Umbilical Vein Endothelial Cells

TL;DR: Results suggest that metformin normalizes hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis through the activation of AMPK-PGC-1alpha pathway.
Journal ArticleDOI

Adenosine Monophosphate-Activated Protein Kinase Suppresses Vascular Smooth Muscle Cell Proliferation Through the Inhibition of Cell Cycle Progression

TL;DR: The data suggest for the first time that AMPK suppresses VSMC proliferation via cell cycle regulation by p53 upregulation and AMPK activation in VSMCs may be a therapoietic target for the prevention of vascular diseases.
Journal ArticleDOI

Evaluation of urinary 8-hydroxydeoxy-guanosine as a novel biomarker of macrovascular complications in type 2 diabetes

TL;DR: Hyperglycemia independently increases 8-OHdG in patients with type 2 diabetes, and this biomarker is a useful biomarker of not only microvascular but also macrovascular complications in Patients withType 2 diabetes.
Journal ArticleDOI

Impact of mitochondrial reactive oxygen species and apoptosis signal-regulating kinase 1 on insulin signaling.

TL;DR: The results suggest that TNF-α increases mitochondrial ROS and activates ASK1 in Huh7 cells and that these T NF-α–induced phenomena contribute, at least in part, to impaired insulin signaling.