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Researcher · Toho University · Japan

Atsuhiko T. Naito

Atsuhiko T. Naito publishes mostly in Molecular Biology, Cardiology and Cardiovascular Medicine and Surgery, on topics such as Cardiac electrophysiology and arrhythmias, Tissue Engineering and Regenerative Medicine and Congenital heart defects research.

ORCID 0000-0003-2534-1920 OpenAlex
World rank
#1,552,353
of 7,710,434 ranked researchers
Rank in Japan
#25,092
of 383,136
Works
126
Citations
4.6k
Citations per work
36.5
h-index
32
i10-index 54Top 13% in Molecular Biology
Atsuhiko T. Naito

What does Atsuhiko T. Naito research?

Atsuhiko T. Naito's work is mostly in Biochemistry, Genetics and Molecular Biology (32%), Medicine (31%), Immunology and Microbiology (3%).

Life Sciences: 48 works · 38.2% of their workBiochemistry, Genetics and Molecular Biology: 41 works · 32.2% of their workMolecular Biology: 41 works · 32.2% of their workImmunology and Microbiology: 4 works · 3.0% of their workImmunology: 4 works · 3.0% of their workNeuroscience: 4 works · 3.0% of their workCellular and Molecular Neuroscience: 4 works · 3.0% of their workHealth Sciences: 39 works · 31.3% of their workMedicine: 39 works · 31.3% of their workCardiology and Cardiovascular Medicine: 28 works · 22.5% of their workSurgery: 8 works · 6.1% of their workPharmacology: 3 works · 2.7% of their workEverything else: 38 works · 30.5% of their workTHEIR WORKAtsuhiko T. Naito126works
Life Sciences38%Health Sciences31%

Their six largest subfields, inside their fields and domains; the grey slice is everything else they publish. The interactive view splits every one of their works down to single topics.

The fields and subfields, with their numbers
    1. Biochemistry, Genetics and Molecular Biology4132.2%
    2. Immunology and Microbiology43.0%
    3. Neuroscience43.0%
    1. Medicine3931.3%
  3. Everything else3830.5%
  1. 1Molecular Biology32% of their works
  2. 2Cardiology and Cardiovascular Medicine22% of their works
  3. 3Surgery6% of their works
  4. 4Immunology3% of their works
  5. 5Cellular and Molecular Neuroscience3% of their works
  6. 6Pharmacology3% of their works

Research topics

Which keywords describe Atsuhiko T. Naito's research?

The keywords of their largest research topics: Ion Channels, Extracellular Matrix, Arrhythmias, Long-QT Syndrome, Wnt Signaling, Cell Signaling, Decellularization and Organ Engineering.

Size is their works in the topics tagged with each word, from their 8 largest topics. Each links to the topic it comes from most. The words come from the keyword list OpenAlex gives each topic, not from the text of the papers, so a word can appear that none of the papers uses.

All 20 words, with their numbers
  1. Ion Channels372 topics
  2. Extracellular Matrix332 topics
  3. Arrhythmias271 topic
  4. Long-QT Syndrome271 topic
  5. Wnt Signaling232 topics
  6. Cell Signaling182 topics
  7. Decellularization181 topic
  8. Organ Engineering181 topic
  9. Cardiomyocyte Renewal161 topic
  10. Heart Regeneration161 topic
  11. Cardiac Remodeling151 topic
  12. Inflammatory Response151 topic
  13. Induced Pluripotent Stem Cells131 topic
  14. Pluripotent Stem Cells131 topic
  15. Calcium Channels101 topic
  16. Voltage-Gated Channels101 topic
  17. Crystal Structure81 topic
  18. G-Protein-Coupled Receptors81 topic
  19. Stem Cells71 topic
  20. ß-Catenin71 topic

Where does Atsuhiko T. Naito work?

Atsuhiko T. Naito's main affiliation in the publication record is Toho University, Japan.

How many publications and citations does Atsuhiko T. Naito have?

OpenAlex counts 126 works and 4,595 citations for Atsuhiko T. Naito, an h-index of 32, ranking #1,552,353 of 7,710,434 researchers worldwide on the quality score.

Ranked on field-normalised citation excellence (50%), output (30%) and citations (20%). Counts come from OpenAlex author records, which occasionally merge different people who share a name or split one person into several.

Papers, co-authors, who cited this work and researchers on the nearest topics have tabs of their own, above. Is this your page? Claim it with your ORCID iD, or request a correction or removal.

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