Hidemi Nonaka
- Endocrine and Autonomic Systems top 2%
- Physiology top 10%
- Cell Biology top 10%
- Molecular Biology
- Cardiology and Cardiovascular Medicine
- Co-authors
- Noriaki EmotoMitsuhiro YokoyamaKazuhiro YagitaHitoshi OkamuraHiroyuki FukuyaTakeshi TsujinoYasuhiro WatariMohammad Saifur Rohman
- Topics
- Circadian rhythm and melatonin (5 papers)Aldose Reductase and Taurine (4 papers)Dietary Effects on Health (3 papers)
- Partner nations
- JapanUnited States
In The Last Decade
Hidemi Nonaka
13 papers receiving 646 citations
Peers
Comparison fields: 5 of 78
- Endocrine and Autonomic Systems 329
- Physiology 305
- Cell Biology 111
- Molecular Biology 106
- Cardiology and Cardiovascular Medicine 89
Countries citing papers authored by Hidemi Nonaka
This map shows the geographic impact of Hidemi Nonaka's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Hidemi Nonaka with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Hidemi Nonaka more than expected).
Fields of papers citing papers by Hidemi Nonaka
This network shows the impact of papers produced by Hidemi Nonaka. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Hidemi Nonaka. The network helps show where Hidemi Nonaka may publish in the future.
Co-authorship network of co-authors of Hidemi Nonaka
This figure shows the co-authorship network connecting the top 25 collaborators of Hidemi Nonaka. A scholar is included among the top collaborators of Hidemi Nonaka based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Hidemi Nonaka. Hidemi Nonaka is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 6 | |
| 2 | 1 | |
| 3 | 70 | |
| 4 | 9 | |
| 5 | PE-209 VEGF Upregulation In Mice Lacking Endothelin-1 In Vascular Endothelial Cell Compensates the Lack of Heart Vascularization on the Expense of Inflammation(Cardiac hypertrophy, basic/clinical-2, The 71st Annual Scientific Meeting of the Japanese Circulation Society) | 1 |
| 6 | 62 | |
| 7 | 94 | |
| 8 | 46 | |
| 9 | 75 | |
| 10 | 9 | |
| 11 | 149 | |
| 12 | 129 | |
| 13 | 25 |
About Hidemi Nonaka
Hidemi Nonaka is a scholar working on Aging, Endocrine and Autonomic Systems and Physiology, having authored 13 papers that have together received 676 indexed citations. Recurring topics across this work include Circadian rhythm and melatonin (5 papers), Aldose Reductase and Taurine (4 papers) and Dietary Effects on Health (3 papers). The work is most often cited by research in Endocrine and Autonomic Systems (329 citations), Aging (62 citations) and Physiology (305 citations). Hidemi Nonaka has collaborated with scholars based in Japan and United States. Frequent co-authors include Noriaki Emoto, Mitsuhiro Yokoyama, Kazuhiro Yagita, Hitoshi Okamura, Hiroyuki Fukuya, Takeshi Tsujino, Yasuhiro Watari, Mohammad Saifur Rohman, Koji Ikeda and Sunu Budhi Raharjo. Their work appears in journals such as Circulation, Biochemical and Biophysical Research Communications and Kidney International.
Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.