Yoshiro Maezawa

ORCID: 0000-0001-5567-9901
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About
Contact & Profiles
Research Areas
  • Diabetes Treatment and Management
  • DNA Repair Mechanisms
  • Nuclear Structure and Function
  • Chronic Kidney Disease and Diabetes
  • RNA regulation and disease
  • Renal Diseases and Glomerulopathies
  • Atherosclerosis and Cardiovascular Diseases
  • Pancreatic function and diabetes
  • Renal and related cancers
  • Metabolism, Diabetes, and Cancer
  • Lipoproteins and Cardiovascular Health
  • Asthma and respiratory diseases
  • Coronary Interventions and Diagnostics
  • Angiogenesis and VEGF in Cancer
  • Diet and metabolism studies
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • IL-33, ST2, and ILC Pathways
  • Nutrition and Health in Aging
  • Congenital heart defects research
  • Diabetes and associated disorders
  • Genetic and Kidney Cyst Diseases
  • Mitochondrial Function and Pathology
  • Adipose Tissue and Metabolism
  • Telomeres, Telomerase, and Senescence
  • Retinal Diseases and Treatments

Chiba University
2016-2025

Chiba University Hospital
2015-2025

International University of Health and Welfare
2019

Japanese Red Cross Narita Hospital
2019

Hospital for Sick Children
2012-2015

SickKids Foundation
2012-2015

University of Toronto
2009-2015

Lunenfeld-Tanenbaum Research Institute
2010-2014

Mount Sinai Hospital
2010-2014

University College London
2013

The IL-23-IL-17A-producing CD4(+) T-cell (Th17 cell) axis plays an important role in the development of chronic inflammatory diseases, including autoimmune diseases. However, IL-23-Th17 cell regulation allergic airway inflammation is still largely unknown.To determine IL-23 and Th17 cells inflammation.We examined effect anti-IL-23 antibody on antigen-induced inflammation. We also investigated enforced expression by generating lung-specific transgenic mice. Moreover, we adoptive transfer...

10.1164/rccm.200801-086oc article EN American Journal of Respiratory and Critical Care Medicine 2008-09-12

Abstract Metabolic dysfunction is a primary feature of Werner syndrome (WS), human premature aging disease caused by mutations in the gene encoding (WRN) DNA helicase. WS patients exhibit severe metabolic phenotypes, but underlying mechanisms are not understood, and whether deficit can be targeted for therapeutic intervention has been determined. Here we report impaired mitophagy depletion NAD + , fundamental ubiquitous molecule, patient samples invertebrate models. WRN regulates...

10.1038/s41467-019-13172-8 article EN cc-by Nature Communications 2019-11-21

Inhibitors of the mammalian target rapamycin (MTOR) belong to a family drugs with potent immunosuppressive, antiangiogenic, and antiproliferative properties. De novo or worsening proteinuria can occur during treatment these agents, but mechanism by which this occurs is unknown. We generated characterized mice carrying podocyte-selective knockout Mtor gene. Although was dispensable in developing podocytes, developed at 3 weeks end stage renal failure 5 after birth. Podocytes from exhibited an...

10.1681/asn.2011070690 article EN Journal of the American Society of Nephrology 2011-12-23

Vascular endothelial growth factor A (VEGFA) expression is increased in glomeruli the context of diabetes. Here, we tested hypothesis that this upregulation VEGFA protects glomerular microvasculature diabetes and therefore inhibition will accelerate nephropathy. To determine role Vegfa development progression diabetic nephropathy, used an inducible Cre-loxP gene-targeting system enabled genetic deletion selectively from podocytes wild-type or mice. Type 1 was induced mice using...

10.2337/db11-1655 article EN cc-by-nc-nd Diabetes 2012-08-14

The search for developmental mechanisms driving vertebrate organogenesis has paved the way toward a deeper understanding of birth defects. During embryogenesis, parts heart and craniofacial muscles arise from pharyngeal mesoderm (PM) progenitors. Here, we reveal hierarchical regulatory network set transcription factors expressed in PM that initiates organogenesis. Genetic perturbation this mice resulted muscle defects, revealing robust cross-regulation between its members. We identified Lhx2...

10.1073/pnas.1208690109 article EN Proceedings of the National Academy of Sciences 2012-10-29

IL-25 (IL-17E) induces IL-4, IL-5, and IL-13 production from an unidentified non-T/non-B cell population subsequently Th2-type immune responses such as IgE eosinophilic airway inflammation. IL-25R is a single transmembrane protein with homology to IL-17R, but the signaling pathways have not been fully understood. In this study, we investigated pathway under IL-25R, especially possible involvement of TNFR-associated factor (TRAF)6 in pathway. We found that cross-linking induced NF-kappaB...

10.4049/jimmunol.176.2.1013 article EN The Journal of Immunology 2006-01-15

The International Mouse Phenotyping Consortium (IMPC) plans to phenotype 20,000 single-gene knockout mice gain an insight into gene function. Approximately 30% of these mouse lines will be embryonic or perinatal lethal. IMPC has selected three-dimensional (3D) imaging at relevant stages development in attempt discover the cause lethality using detailed anatomical information. Rate throughput is paramount as production centers have been given ambitious task completing this phenotyping project...

10.1242/dev.107722 article EN Development 2014-05-22

Podocytes are terminally differentiated cells with an elaborate cytoskeleton and critical components of the glomerular barrier. We identified a bHLH transcription factor, Tcf21, that is highly expressed in developing mature podocytes. Because conventional Tcf21 knockout mice die perinatal period major cardiopulmonary defects, we generated conditional mouse to explore role this factor podocytes vivo. was deleted from podocyte progenitors using podocin-cre (podTcf21) wnt4-cre (wnt4creTcf21)...

10.1681/asn.2013121307 article EN Journal of the American Society of Nephrology 2014-06-06

The role of transforming growth factor (TGF)-beta and its signal in atherogenesis is not fully understood. Here, we examined mice lacking Smad3, a major downstream mediator TGF-beta, to clarify the precise Smad3-dependent signaling vascular response injury. Femoral arteries were injured wild-type Smad3-null (null) male on C57Bl/6 background. Histopathological evaluation 1 3 weeks after injury revealed significant enhancement neointimal hyperplasia null compared with mice. Transplantation...

10.1161/01.res.0000163980.55495.44 article EN Circulation Research 2005-03-25

A prospective, multicentre, open-label, blinded-endpoint, randomized controlled study was conducted to evaluate the efficacy of treatment with ipragliflozin (sodium-dependent glucose transporter-2 inhibitor) versus metformin for visceral fat reduction and glycaemic control among Japanese patients type 2 diabetes treated sitagliptin, HbA1c levels 7%-10%, body mass index (BMI) ≥ 22 kg/m2 . Patients were randomly assigned (1:1) receive 50 mg or 1000-1500 daily. The primary outcome change in...

10.1111/dom.13750 article EN cc-by Diabetes Obesity and Metabolism 2019-04-17

Senescent cells exhibit several typical features, including the senescence-associated secretory phenotype (SASP), promoting secretion of various inflammatory proteins and small extracellular vesicles (EVs). SASP factors cause chronic inflammation, leading to age-related diseases. Recently, therapeutic strategies targeting senescent cells, known as senolytics, have gained attention; however, noninvasive methods detect in living organisms not been established. Therefore, goal this study was...

10.3390/ijms24032421 article EN International Journal of Molecular Sciences 2023-01-26

Werner syndrome (WS), caused by mutations in the RecQ helicase WERNER (WRN) gene, is a classical accelerated aging disease with patients suffering from several metabolic dysfunctions without cure. While, as we previously reported, depleted NAD+ causes accumulation of damaged mitochondria, leading to compromised metabolism, how mitochondrial changes WS and impact on pathologies were unknown. We show that loss WRN increases senescence mesenchymal stem cells (MSCs) likely related dysregulation...

10.18632/aging.206236 article EN cc-by Aging 2025-04-02
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