Yasuko Iwakiri

ORCID: 0000-0001-8032-5654
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About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Liver Disease and Transplantation
  • Liver physiology and pathology
  • Nitric Oxide and Endothelin Effects
  • Organ Transplantation Techniques and Outcomes
  • Lymphatic System and Diseases
  • Eicosanoids and Hypertension Pharmacology
  • Alcohol Consumption and Health Effects
  • Endoplasmic Reticulum Stress and Disease
  • Genetic and Kidney Cyst Diseases
  • Diet, Metabolism, and Disease
  • Pancreatic function and diabetes
  • Phagocytosis and Immune Regulation
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Hepatitis C virus research
  • Cerebrospinal fluid and hydrocephalus
  • MicroRNA in disease regulation
  • Lymphatic Disorders and Treatments
  • Fatty Acid Research and Health
  • Lipid metabolism and disorders
  • Epigenetics and DNA Methylation
  • Macrophage Migration Inhibitory Factor
  • Atherosclerosis and Cardiovascular Diseases
  • Angiogenesis and VEGF in Cancer

Yale University
2016-2025

Centre For Digestive Diseases
2006-2019

Kitasato University
2014

Park Plaza Hospital
2012

Level (Czechia)
2012

University of New Haven
2012

National Institutes of Health
2007

VA Connecticut Healthcare System
2002-2007

King Saud University
2007

Riyadh Armed Forces Hospital
2007

Dysfunction of liver sinusoidal endothelial cells (LSECs) is permissive for the progression fibrosis and cirrhosis responsible its clinical complications. Here, we have mapped spatial distribution heterogeneous ECs in normal vs cirrhotic mouse livers identified zone-specific transcriptomic changes LSECs associated with using scRNA-seq technology.

10.1016/j.jcmgh.2020.12.007 article EN cc-by-nc-nd Cellular and Molecular Gastroenterology and Hepatology 2020-12-17

Nitric oxide (NO) is a highly diffusible and short-lived physiological messenger. Despite its nature, NO modifies thiol groups of specific cysteine residues in target proteins alters protein function via S-nitrosylation. Although intracellular S-nitrosylation posttranslational modification, the defined localization an source (nitric synthase, NOS) with has never been directly demonstrated. Endothelial NOS (eNOS) localized mainly on Golgi apparatus plasma membrane caveolae. Here, we show by...

10.1073/pnas.0605907103 article EN Proceedings of the National Academy of Sciences 2006-12-15

Increased nitric oxide (NO) is the main factor leading to hyperdynamic circulation associated with advanced portal hypertension (PHT), but initial mechanisms and magnitude of increase in pressure required trigger NO production are not known. We addressed these issues by studying systemic splanchnic hemodynamics endothelial synthase (eNOS) VEGF expression rats different degrees hypertension. Portal vein ligation (PVL) performed over needles three calibers (16-, 18-, 20-gauge) yielded PHT...

10.1152/ajpgi.00336.2005 article EN AJP Gastrointestinal and Liver Physiology 2006-04-07

Transient disruption of endothelial adherens junctions and cytoskeletal remodeling are responsible for increases in vascular permeability induced by inflammatory stimuli growth factor (VEGF). Nitric oxide (NO) produced NO synthase (eNOS) is critical VEGF changes vivo, however, the molecular mechanisms which endogenous modulates not clear. Here we show that lack eNOS reduces permeability, an effect mediated enhanced Rac-GTPase activation stabilization cortical actin. The loss NO, increased...

10.1242/jcs.115972 article EN Journal of Cell Science 2013-01-01

Highlights•Liver injury in patients with COVID-19 is associated elevated IL-6 and coagulopathy.•Patients exhibit hepatic endotheliopathy which liver injury.•IL-6 trans-signaling causes sinusoidal endothelial cells.AbstractBackground AimsCOVID-19 interleukin-6 (IL-6). We hypothesized that cells (LSECs) leads to (a proinflammatory procoagulant state) COVID-19.MethodsCoagulopathy, endotheliopathy, alanine aminotransferase (ALT) were retrospectively analyzed a subset (n = 68), followed by larger...

10.1016/j.jhep.2021.04.050 article EN other-oa Journal of Hepatology 2021-05-13

Worldwide, over a billion people suffer from chronic liver diseases, which often lead to fibrosis and then cirrhosis. Treatments for remain experimental, in part because no unifying mechanism has been identified that initiates fibrosis. Necroptosis implicated multiple diseases. Here, we report O-linked β-N-acetylglucosamine (O-GlcNAc) modification protects against hepatocyte necroptosis initiation of Decreased O-GlcNAc levels were seen patients with alcoholic cirrhosis mice ethanol-induced...

10.1172/jci.insight.127709 article EN JCI Insight 2019-10-31
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