Hiroshi Akazawa

ORCID: 0000-0002-3574-9607
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About
Contact & Profiles
Research Areas
  • Cardiac Fibrosis and Remodeling
  • Receptor Mechanisms and Signaling
  • Congenital heart defects research
  • Signaling Pathways in Disease
  • Cardiac electrophysiology and arrhythmias
  • Renin-Angiotensin System Studies
  • Adipose Tissue and Metabolism
  • Cardiomyopathy and Myosin Studies
  • Connective tissue disorders research
  • Cardiovascular Function and Risk Factors
  • Ion channel regulation and function
  • Tissue Engineering and Regenerative Medicine
  • Cardiac Imaging and Diagnostics
  • Oral microbiology and periodontitis research
  • Chemotherapy-induced cardiotoxicity and mitigation
  • Mitochondrial Function and Pathology
  • Aortic Disease and Treatment Approaches
  • Aortic aneurysm repair treatments
  • Heart Failure Treatment and Management
  • Cancer Treatment and Pharmacology
  • RNA Research and Splicing
  • Cardiac Ischemia and Reperfusion
  • Cardiovascular Effects of Exercise
  • Hormonal Regulation and Hypertension
  • Heat shock proteins research

The University of Tokyo
2016-2025

University of Tokyo Hospital
2015-2024

Japan Agency for Medical Research and Development
2015-2018

Tokyo Medical University
2018

Osaka University
2010-2017

Tokyo Medical and Dental University
2017

Japan Science and Technology Agency
2000-2015

Kansai Medical University
2015

Kyushu University
2008-2015

Shinshu University
2013

Although somatic stem cells have been reported to exist in various adult organs, there few reports concerning the heart. We here demonstrate that Sca-1-positive (Sca-1+) hearts some of features cells. Sca-1+ were isolated from murine by a magnetic cell sorting system and cultured on gelatin-coated dishes. A fraction stuck culture dish proliferated slowly. When treated with oxytocin, expressed genes cardiac transcription factors contractile proteins showed sarcomeric structure spontaneous...

10.1074/jbc.m310822200 article EN cc-by Journal of Biological Chemistry 2004-03-01

Although Wingless (Wg)/Wnt signaling has been implicated in heart development of multiple organisms, conflicting results have reported regarding the role Wnt/beta-catenin pathway cardiac myogenesis: Wg/armadillo promotes Drosophila, whereas activation inhibits formation avians and amphibians. Using an vitro system mouse ES cell differentiation into cardiomyocytes, we show here that exhibits developmental stage-specific, biphasic, antagonistic effects on cardiomyogenesis...

10.1073/pnas.0605768103 article EN Proceedings of the National Academy of Sciences 2006-12-15

Side population (SP) cells, which can be identified by their ability to exclude Hoechst 33342 dye, are one of the candidates for somatic stem cells. Although bone marrow SP cells known long-term repopulating hematopoietic there is little information about characteristics cardiac (CSPs). When cultured CSPs from neonatal rat hearts were treated with oxytocin or trichostatin A, some expressed cardiac-specific genes and proteins showed spontaneous beating. green fluorescent protein–positive...

10.1083/jcb.200603014 article EN The Journal of Cell Biology 2007-01-29

Pressure overload induces a transition from cardiac hypertrophy to heart failure, but its underlying mechanisms remain elusive. Here we reconstruct trajectory of cardiomyocyte remodeling and clarify distinct gene programs encoding morphological functional signatures in by integrating single-cardiomyocyte transcriptome with cell morphology, epigenomic state function. During early hypertrophy, cardiomyocytes activate mitochondrial translation/metabolism genes, whose expression is correlated...

10.1038/s41467-018-06639-7 article EN cc-by Nature Communications 2018-10-19

Emerging evidence has suggested a potential impact of gut microbiota on the pathophysiology heart failure (HF). However, it is still unknown whether HF associated with dysbiosis in microbiota. We investigated composition patients to elucidate microbial HF. performed 16S ribosomal RNA gene sequencing fecal samples obtained from 12 and age-matched healthy control (HC) subjects, analyzed differences further compared younger than 60 years age that 10 or older. The communities was distinct HC...

10.1371/journal.pone.0174099 article EN cc-by PLoS ONE 2017-03-22

Although many animal studies indicate insulin has cardioprotective effects, clinical suggest a link between resistance (hyperinsulinemia) and heart failure (HF). Here we have demonstrated that excessive cardiac signaling exacerbates systolic dysfunction induced by pressure overload in rodents. Chronic hepatic plasma level elevation. In contrast, was upregulated chronic because of mechanical stretch-induced activation cardiomyocyte receptors upregulation receptor Irs1 expression. increased...

10.1172/jci40096 article EN Journal of Clinical Investigation 2010-04-20

Mechanical stress activates various hypertrophic responses, including activation of mitogen-activated protein kinases (MAPKs) in cardiac myocytes. Stretch activated extracellular signal-regulated partly through secreted humoral growth factors, angiotensin II, whereas stretch-induced c-Jun NH(2)-terminal and p38 MAPK was independent II. In this study, we examined the role integrin signaling cardiomyocytes neonatal rats. Overexpression tumor suppressor PTEN, which inhibits outside-in...

10.1161/hy0202.102699 article EN Hypertension 2002-02-01

Pretreatment with a combination of granulocyte colony-stimulating factor (G-CSF) and stem cell (SCF) has been reported to attenuate left ventricular (LV) remodeling after acute myocardial infarction (MI). We here examined whether the cytokine treatment started MI also beneficial effects. Anterior was created in recipient mice whose bone marrow had replaced that transgenic expressing enhanced green fluorescent protein (GFP). categorized into five groups according following treatment: 1)...

10.1096/fj.03-0637fje article EN The FASEB Journal 2004-03-04

Atrial fibrillation (AF) is a common arrhythmia that increases the risk of stroke and heart failure. Here, we have shown mast cells, key mediators allergic immune responses, are critically involved in AF pathogenesis stressed mouse hearts. Pressure overload induced cell infiltration fibrosis atrium enhanced susceptibility following atrial burst stimulation. Both inducibility were attenuated by stabilization cells with cromolyn BM reconstitution from cell-deficient WBB6F1-KitW/W-v mice. When...

10.1172/jci39942 article EN Journal of Clinical Investigation 2009-12-28

The discovery of bone marrow–derived endothelial progenitors in the peripheral blood has promoted intensive studies on potential cell therapy for various human diseases. Accumulating evidence suggested that implantation marrow mononuclear cells effectively promotes neovascularization ischemic tissues. It also been reported implanted are incorporated not only into newly formed vessels but secrete angiogenic factors. However, mechanism by which improves tissue ischemia remains obscure. We...

10.1161/01.res.0000219901.13974.15 article EN Circulation Research 2006-03-31

Rationale : The number of patients with coronary heart disease, including myocardial infarction, is increasing and novel therapeutic strategy awaited. Tumor suppressor protein p53 accumulates in the myocardium after causes apoptosis cardiomyocytes, plays an important role progression into failure. Objectives We investigated molecular mechanisms accumulation infarction tested whether anti-p53 approach would be effective against infarction. Methods Results Through expression screening, we...

10.1161/circresaha.109.214346 article EN Circulation Research 2010-04-23

Abstract The DNA damage response (DDR) plays a pivotal role in maintaining genome integrity. and DDR activation are observed the failing heart, however, type of its pathogenesis heart failure remain elusive. Here we show critical single-strand break (SSB) pressure overload-induced failure. Accumulation unrepaired SSB is cardiomyocytes heart. Unrepaired activates increases expression inflammatory cytokines through NF-κB signalling. Pressure more severe mice lacking XRCC1, an essential protein...

10.1038/ncomms15104 article EN cc-by Nature Communications 2017-04-24
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