Satoshi Matsuzaki

ORCID: 0009-0009-1846-3429
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Adipose Tissue and Metabolism
  • Cardiovascular Function and Risk Factors
  • Metabolism, Diabetes, and Cancer
  • Spectroscopy and Quantum Chemical Studies
  • Kawasaki Disease and Coronary Complications
  • ATP Synthase and ATPases Research
  • Diet and metabolism studies
  • Photosynthetic Processes and Mechanisms
  • Cancer, Hypoxia, and Metabolism
  • Cardiac Ischemia and Reperfusion
  • Coronary Artery Anomalies
  • Neurotransmitter Receptor Influence on Behavior
  • Probabilistic and Robust Engineering Design
  • Acute Myeloid Leukemia Research
  • Fatigue and fracture mechanics
  • Photoreceptor and optogenetics research
  • Photochemistry and Electron Transfer Studies
  • Cardiovascular Issues in Pregnancy
  • Neuroscience and Neuropharmacology Research
  • Cardiac Structural Anomalies and Repair
  • Electron Spin Resonance Studies
  • Mechanical Circulatory Support Devices
  • Receptor Mechanisms and Signaling
  • Diet, Metabolism, and Disease

Oklahoma Medical Research Foundation
2016-2025

Osaka Dental University
2021

Aarhus University
2021

Center for Neurosciences
2021

Shinshu University
1983-2019

University of Oklahoma Health Sciences Center
2006-2018

Ōtani University
2016

Iowa State University
2000-2006

Kansas State University
2006

Nihon University
2002-2005

Early reperfusion of ischemic cardiac tissue remains the most effective intervention for improving clinical outcome following myocardial infarction. However, abnormal increases in intracellular Ca²⁺ during can cause cardiomyocyte death and consequent loss function, referred to as ischemia/reperfusion (IR) injury. Therapeutic modulation handling provides some cardioprotection against paradoxical effects restoring blood flow heart, highlighting significance overload IR Cardiac is also...

10.1172/jci59327 article EN Journal of Clinical Investigation 2012-03-19

Histone deacetylase (HDAC) inhibitors show remarkable therapeutic potential for a variety of disorders, including cancer, neurological disease, and cardiac hypertrophy. However, the specific HDAC isoforms that mediate their actions are unclear, as physiological pathological functions individual HDACs in vivo. To explore role Hdac3 heart, we generated mice with conditional null allele. Although global deletion resulted lethality by E9.5, cardiac-specific survived until 3-4 months age. At this...

10.1172/jci35847 article EN Journal of Clinical Investigation 2008-10-15

10.1016/0027-5107(85)90109-5 article EN Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 1985-06-01

A decline in mitochondrial function and biogenesis as well increased reactive oxygen species (ROS) are important determinants of aging. With advancing age, there is a concomitant reduction circulating levels insulin-like growth factor-1 (IGF-1) that closely associated with neuronal aging neurodegeneration. In this study, we investigated the effect IGF-1 signaling age on astrocyte metabolism its association learning memory.Learning memory was assessed using radial arm water maze young old...

10.1016/j.molmet.2018.01.013 article EN cc-by-nc-nd Molecular Metabolism 2018-02-02

Few studies with sufficient statistical power have shown the association of z score coronary arterial internal diameter events (CE) in patients Kawasaki disease (KD) artery aneurysms (CAA).To clarify time-dependent CE occurrence KD CAA.This multicenter, collaborative retrospective cohort study 44 participating institutions included 1006 younger than 19 years who received a angiography between 1992 and 2011.The CE, including thrombosis, stenosis, obstruction, acute ischemic events,...

10.1001/jamapediatrics.2018.0030 article EN JAMA Pediatrics 2018-03-05

Biguanides are widely used antihyperglycemic agents for diabetes mellitus and prediabetes treatment. Complex I is the rate-limiting step of mitochondrial electron transport chain (ETC), a major source free radical production, known target biguanides. has two reversible conformational states, active de-active. The deactivated state promoted in absence substrates but rapidly fully reversed to presence NADH. objective this study was determine relative sensitivity active/de-active complex...

10.1021/bi501473h article EN Biochemistry 2015-02-26

Abstract Background Excess reactive oxygen species (ROS) and muscle weakness occur in parallel multiple pathological conditions. However, the causative role of skeletal mitochondrial ROS (mtROS) on neuromuscular junction (NMJ) morphology function has not been directly investigated. Methods We generated mice lacking muscle‐specific manganese‐superoxide dismutase (m Sod2 KO) to increase mtROS using a cre‐Lox approach driven by human actin. determined primary functional parameters (respiration,...

10.1002/jcsm.12375 article EN cc-by-nc Journal of Cachexia Sarcopenia and Muscle 2019-02-01

Mice lacking Epas1, encoding the transcription factor Hypoxia-inducible Factor 2alpha (HIF-2alpha), exhibit an apparent mitochondrial disease state. Similarities between knock-outs of Epas1 and Sod2, antioxidant enzyme manganese superoxide dismutase, led to identification Sod2 as a HIF-2alpha target gene. However, levels in Epas1(-)(/)(-) liver are intermediate that Sod(+)(/)(-) Sod2(-)(/)(-) mice, which have subtle or severe phenotypes, respectively. This suggests additional genes besides...

10.1074/jbc.m611133200 article EN cc-by Journal of Biological Chemistry 2007-02-24

Background Coronary arterial aneurysms (CAAs) associated with Kawasaki disease (KD) significantly affect prognosis. However, the clinical course of CAAs and factors CAA regression have not been well analyzed. Methods Results The cohort Z-Score 2nd Project Stage study, a multicenter, retrospective, study involving 44 institutions in Japan including 1006 patients KD, was examined. were classified by z score their internal diameter acute phase: small (z<5), medium (5≤z<10), large (z≥10). lower...

10.1161/jaha.121.022417 article EN cc-by-nc-nd Journal of the American Heart Association 2023-01-31

Diabetes is associated with a cardiomyopathy that independent of coronary artery disease or hypertension. In the present study we used in vivo magnetic resonance imaging (MRI) and echocardiographic techniques to examine characterize early changes myocardial function mouse model type 1 diabetes. was induced 8-week old C57BL/6 mice two intraperitoneal injections streptozotocin. The blood glucose levels were maintained at 19–25 mmol/l using intermittent low dosages long acting insulin glargine....

10.1186/1475-2840-6-6 article EN cc-by Cardiovascular Diabetology 2007-01-01

Diabetic cardiomyopathy refers to the changes in contractility that occur diabetic heart can arise absence of vascular disease. Mitochondrial bioenergetic deficits and increased free radical production are pathological hallmarks cardiomyopathy, but mechanisms causal relationships between mitochondrial progression disease not understood. We evaluated cardiac function a rodent model chronic Type 1 diabetes (OVE26 mice) before onset deficits. found most pronounced change OVE26 mitochondria is...

10.1042/bj20121038 article EN Biochemical Journal 2012-10-04

The healthy heart has a dynamic capacity to respond and adapt changes in nutrient availability. Diabetes mellitus disrupts this metabolic flexibility promotes cardiomyopathy through mechanisms that are not completely understood. Phosphofructokinase 2 (PFK-2) is primary regulator of cardiac glycolysis substrate selection, yet its regulation under normal pathological conditions unknown. This study was undertaken determine how insulin signaling affect PFK-2 content, activity,...

10.1161/jaha.117.007159 article EN cc-by-nc-nd Journal of the American Heart Association 2017-12-02

10.1016/j.jpeds.2017.10.013 article EN The Journal of Pediatrics 2017-12-07

Diabetic retinopathy (DR) is a common neurovascular complication of type 1 diabetes. Current therapeutics target neovascularization characteristic end-stage disease, but are associated with significant adverse effects. Targeting early events DR such as neurodegeneration may lead to safer and more effective approaches treatment. Two independent prospective clinical trials unexpectedly identified that the PPARα agonist fenofibrate had unprecedented therapeutic effects in DR, gave little...

10.1371/journal.pone.0208399 article EN cc-by PLoS ONE 2019-02-04

To determine whether the acute cardiac depressant effects of ethanol could be attributed to its metabolite (acetaldehyde), either or acetaldehyde was intravenously infused into pentobarbital anaesthetised, closed-chest dogs. At a venous blood level 199±43 (SE) mg·dl−1, ejection fraction had decreased from 35±2 30±2%, P <0.05, max dP/dt/end-diastolic volume 14.0±2.1 8.6 ± 1.1 kPa·s−1·cm−3 (105 16 65±8 mmHg·s−1·cm−3), P<0.02, whereas end-diastolic (P <0.005), myocardial oxygen consumption...

10.1093/cvr/13.8.477 article EN Cardiovascular Research 1979-08-01

The antenna chlorophyll a (Chl a) molecules of photosystem I green plants and cyanobacteria that absorb further to the red than P700, special pair reaction center, have long been considerable interest. Recently, results nonphotochemical hole burning experiments at liquid helium temperatures, which included use high pressure external electric (Stark) fields, led conclusion cyanobacterium Synechocystis sp. PCC 6803 possesses two "red" states whose S0 (ground state) → Qy(S1) origin absorption...

10.1021/jp000447u article EN The Journal of Physical Chemistry B 2000-05-19

The CP43 chlorophyll a-core protein complex plays an important role in funneling excitation energy absorbed by more peripheral antenna complexes of photosystem II (PSII) to the reaction center (RC). Identification and characterization lowest Qy-states is for understanding kinetics transfer (EET) from RC. We report results several types spectroscopic experiments performed at liquid He temperatures on isolated spinach. Nonphotochemical hole burning (NPHB) triplet bottleneck spectroscopies as...

10.1021/jp0025431 article EN The Journal of Physical Chemistry B 2000-11-16

Background Phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase (PFK‐2) is a critical glycolytic regulator responsible for upregulation of glycolysis in response to insulin and adrenergic signaling. PFKFB2, the cardiac isoform PFK‐2, degraded heart absence signaling, contributing diabetes‐induced metabolic inflexibility. However, previous studies have not examined how loss PFKFB2 affects global metabolism function. Methods Results To address this, we generated mouse model with...

10.1161/jaha.123.033676 article EN Journal of the American Heart Association 2024-03-27
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