Koji Ohashi

ORCID: 0000-0002-9666-026X
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About
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Research Areas
  • Adipokines, Inflammation, and Metabolic Diseases
  • Adipose Tissue and Metabolism
  • Cardiovascular Disease and Adiposity
  • Diet, Metabolism, and Disease
  • Diet and metabolism studies
  • Birth, Development, and Health
  • Liver Disease Diagnosis and Treatment
  • MicroRNA in disease regulation
  • Epigenetics and DNA Methylation
  • Circular RNAs in diseases
  • Cancer-related molecular mechanisms research
  • Cardiac Fibrosis and Remodeling
  • Embedded Systems Design Techniques
  • Lipid metabolism and disorders
  • Interconnection Networks and Systems
  • Cancer, Hypoxia, and Metabolism
  • Stress Responses and Cortisol
  • Cardiovascular Function and Risk Factors
  • Vitamin C and Antioxidants Research
  • Blood properties and coagulation
  • Fibroblast Growth Factor Research
  • Signaling Pathways in Disease
  • Muscle Physiology and Disorders
  • Regulation of Appetite and Obesity
  • Angiogenesis and VEGF in Cancer

Nagoya University
2016-2025

Fujita Health University
2015-2024

Fujita Health University Hospital
2019-2024

Toyohashi Sozo College
2023

Aichi University
2021

University of Medical Sciences and Technology
2015

RMIT University
2013-2015

Juntendo University
2015

Boston University
2006-2012

Cardiovascular Institute of the South
2010

Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development atherosclerosis. We previously reported that adiponectin, adipocyte-specific plasma protein, accumulated injured artery from and suppressed endothelial inflammatory response vascular smooth muscle cell proliferation, as well macrophage-to-foam transformation vitro. The current study investigated whether increased adiponectin could actually reduce atherosclerosis vivo.Apolipoprotein E-deficient...

10.1161/01.cir.0000042707.50032.19 article EN Circulation 2002-11-25

Background— High-sensitive C-reactive protein (hs-CRP) is a well-known risk factor for coronary artery disease (CAD). Recently, we have demonstrated that adiponectin served as an antiatherogenic plasma which was secreted specifically from adipocytes. The present study investigated the association between and CRP in blood stream adipose tissue. Methods Results— We studied total of 101 male patients, 71 whom had angiographically documented atherosclerosis. As control group, 30 patients with...

10.1161/01.cir.0000055188.83694.b3 article EN Circulation 2003-02-11

Adiponectin is one of the key molecules in metabolic syndrome, and its concentration decreased obesity, type-2 diabetes, coronary artery disease. Genetic investigation has revealed that 2 polymorphisms (I164T G276T) are related to adiponectin diabetes. To examine whether affects hypertension genetically or biologically, we performed a case-control study. A total 446 diagnosed cases (HT) men 312 normotensive (NT) were enrolled this Plasma was measured using an enzyme-linked immunosorbent...

10.1161/01.hyp.0000129281.03801.4b article EN Hypertension 2004-05-04

Endothelial dysfunction is a crucial feature in the evolution of atherosclerosis. Adiponectin an adipocyte-specific plasma protein with antiatherogenic and antidiabetic properties. In present study, we investigated relation between adiponectin endothelium-dependent vasodilation. We analyzed endothelial function 202 hypertensive patients, including those who were not taking any medication. Forearm blood flow was measured by strain-gauge plethysmography. Plasma level highly correlated...

10.1161/01.hyp.0000083488.67550.b8 article EN Hypertension 2003-07-15

Background— Vascular inflammation and subsequent matrix degradation play an important role in the development of atherosclerosis. We previously reported that adiponectin, adipose-specific plasma protein, accumulated to injured artery attenuated vascular inflammatory response. Clinically, high adiponectin level was associated with low cardiovascular event rate patients chronic renal failure. The present study designed elucidate effects on metalloproteinases (MMPs) tissue inhibitor (TIMPs)...

10.1161/01.cir.0000127953.98131.ed article EN Circulation 2004-04-20

Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a previously linked the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression perturbed in models obesity type 2 diabetes. Sfrp5-deficient mice fed high-calorie diet developed severe intolerance hepatic steatosis, their adipose showed accumulation activated macrophages was associated...

10.1126/science.1188280 article EN Science 2010-06-18

Patients with obesity are susceptible to hypertension. We have reported that the plasma adiponectin levels decreased in and has many defensive properties against obesity-related diseases, such as type 2 diabetes coronary artery disease. The aim of this study was determine relationship between hypertension mice. measured blood pressure heart rate directly by a catheter carotid indirectly automatic sphygmomanometer at tail artery. Obese KKAy mice had significantly lower higher systolic than...

10.1161/01.hyp.0000222368.43759.a1 article EN Hypertension 2006-05-02

Myogenic Akt signaling coordinates blood vessel recruitment with normal tissue growth. Here, we investigated the role of Follistatin-like 1 (Fstl1) in regulation endothelial cell function and growth muscle. Transgenic Akt1 overexpression skeletal muscle led to myofiber that was coupled an increase capillary density. or ischemic hind limb surgery induction Fstl1 increased circulating levels Fstl1. Intramuscular administration adenoviral vector expressing (Ad-Fstl1) accelerated flow recovery...

10.1074/jbc.m803440200 article EN cc-by Journal of Biological Chemistry 2008-08-22

Objective— Obesity is recognized increasingly as a major risk factor for kidney disease. We reported previously that plasma adiponectin levels were decreased in obesity, and had defensive properties against type 2 diabetes hypertension. In this study, we investigated the role of disease subtotal nephrectomized mouse model. Methods Results— Subtotal (5/6) nephrectomy was performed adiponectin-knockout (APN-KO) wild-type (WT) mice. The procedure resulted significant accumulation glomeruli...

10.1161/atvbaha.107.147645 article EN Arteriosclerosis Thrombosis and Vascular Biology 2007-07-13

Objectives— Adiponectin is recognized as an antidiabetic, antiatherosclerotic, and anti-inflammatory protein derived from adipocytes. However, the role of adiponectin in cardiac fibrosis remains uncertain. We herein explore effects on induced by angiotensin II (Ang II). Methods Results— Wild-type (WT), knockout (Adipo-KO), PPAR-α (PPAR-α-KO) mice were infused with Ang at 1.2 mg/kg/d. Severe left ventricular dysfunction observed II–infused Adipo-KO compared to WT mice. Adenovirus-mediated...

10.1161/atvbaha.107.156687 article EN Arteriosclerosis Thrombosis and Vascular Biology 2008-02-29

Background— Acute coronary syndrome is a leading cause of death in developed countries. Follistatin-like 1 (FSTL1) myocyte-derived secreted protein that upregulated the heart response to ischemic insult. Here, we investigated therapeutic impact FSTL1 on acute cardiac injury small and large preclinical animal models ischemia/reperfusion dissected its molecular mechanism. Methods Results— Administration human significantly attenuated myocardial infarct size mouse or pig model...

10.1161/circulationaha.112.115089 article EN Circulation 2012-08-29

Rationale: Physical exercise provides benefits for various organ systems, and some of systemic effects are mediated through modulation muscle-derived secreted factors, also known as myokines. Myonectin/C1q (complement component 1q)/TNF (tumor necrosis factor)-related protein 15/erythroferrone is a myokine that upregulated in skeletal muscle blood by exercise. Objective: We investigated the role myonectin myocardial ischemic injury. Methods Results: Ischemia-reperfusion myonectin-knockout...

10.1161/circresaha.118.313777 article EN Circulation Research 2018-12-06
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