Chu Kataoka

1.5k total citations
17 papers, 1.3k citations indexed

About

Chu Kataoka is a scholar working on Immunology, Cardiology and Cardiovascular Medicine and Physiology. According to data from OpenAlex, Chu Kataoka has authored 17 papers receiving a total of 1.3k indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Immunology, 7 papers in Cardiology and Cardiovascular Medicine and 7 papers in Physiology. Recurrent topics in Chu Kataoka's work include Atherosclerosis and Cardiovascular Diseases (8 papers), Nitric Oxide and Endothelin Effects (6 papers) and Angiogenesis and VEGF in Cancer (3 papers). Chu Kataoka is often cited by papers focused on Atherosclerosis and Cardiovascular Diseases (8 papers), Nitric Oxide and Endothelin Effects (6 papers) and Angiogenesis and VEGF in Cancer (3 papers). Chu Kataoka collaborates with scholars based in Japan, United States and Poland. Chu Kataoka's co-authors include Kensuke Egashira, Akira Takeshita, Shiro Kitamoto, Masamichi Koyanagi, Shujiro Inoue, Makoto Usui, Weihua Ni, Makoto Katoh, Hiroaki Shimokawa and Chiyuki Akiyama and has published in prestigious journals such as Circulation, Circulation Research and The FASEB Journal.

In The Last Decade

Chu Kataoka

17 papers receiving 1.3k citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Chu Kataoka Japan 14 390 389 334 312 262 17 1.3k
Annalisa Iezzi Italy 15 326 0.8× 461 1.2× 426 1.3× 399 1.3× 168 0.6× 19 1.8k
Roger Kranzhöfer Germany 15 418 1.1× 404 1.0× 681 2.0× 394 1.3× 177 0.7× 23 1.9k
Yukihiro Hojo Japan 25 604 1.5× 280 0.7× 659 2.0× 369 1.2× 205 0.8× 56 1.6k
Taiki Tojo Japan 20 690 1.8× 523 1.3× 306 0.9× 269 0.9× 172 0.7× 62 1.7k
Jan‐Willem N. Akkerman Netherlands 26 580 1.5× 275 0.7× 553 1.7× 352 1.1× 107 0.4× 59 1.9k
Suzanne J.A. Korporaal Netherlands 22 341 0.9× 258 0.7× 382 1.1× 491 1.6× 171 0.7× 51 1.5k
Alykhan Motani United States 13 764 2.0× 217 0.6× 295 0.9× 293 0.9× 124 0.5× 18 1.5k
Amy Mohan United States 20 762 2.0× 373 1.0× 365 1.1× 260 0.8× 144 0.5× 28 1.4k
Keyvan Mahboubi United States 15 700 1.8× 331 0.9× 205 0.6× 119 0.4× 284 1.1× 22 1.3k
Repin Vs Russia 22 511 1.3× 234 0.6× 189 0.6× 460 1.5× 100 0.4× 136 1.5k

Countries citing papers authored by Chu Kataoka

Since Specialization
Citations

This map shows the geographic impact of Chu Kataoka'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 Chu Kataoka with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Chu Kataoka more than expected).

Fields of papers citing papers by Chu Kataoka

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Chu Kataoka. 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 Chu Kataoka. The network helps show where Chu Kataoka may publish in the future.

Co-authorship network of co-authors of Chu Kataoka

This figure shows the co-authorship network connecting the top 25 collaborators of Chu Kataoka. A scholar is included among the top collaborators of Chu Kataoka 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 Chu Kataoka. Chu Kataoka is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

17 of 17 papers shown
1.
Kataoka, Chu, Kensuke Egashira, Minako Ishibashi, et al.. (2004). Novel anti-inflammatory actions of amlodipine in a rat model of arteriosclerosis induced by long-term inhibition of nitric oxide synthesis. American Journal of Physiology-Heart and Circulatory Physiology. 286(2). H768–H774. 55 indexed citations
2.
Usui, Makoto, Kensuke Egashira, Kisho Ohtani, et al.. (2002). Anti-monocyte chemoattractant protein-1 gene therapy inhibits neointimal hyperplasia after balloon angioplasty in rats and monkeys. Japanese Circulation Journal-english Edition. 66. 702. 1 indexed citations
3.
Ni, Weihua, Kensuke Egashira, Shiro Kitamoto, et al.. (2002). Anti-Monocyte Chemoattractant Protein-1 Gene Therapy Limits Progression and Destabilization of Established Atherosclerosis in Apolipoprotein E-Knockout Mice. Japanese Circulation Journal-english Edition. 66. 704. 1 indexed citations
5.
Egashira, Kensuke, Qingwei Zhao, Chu Kataoka, et al.. (2002). Importance of Monocyte Chemoattractant Protein-1 Pathway in Neointimal Hyperplasia After Periarterial Injury in Mice and Monkeys. Circulation Research. 90(11). 1167–1172. 151 indexed citations
6.
Usui, Makoto, Kensuke Egashira, Kisho Ohtani, et al.. (2002). Anti‐monocyte chemoattractant protein‐1 gene therapy inhibits restenotic changes (neointimal hyperplasia) after balloon injury in rats and monkeys. The FASEB Journal. 16(13). 1–17. 77 indexed citations
7.
Kataoka, Chu, Kensuke Egashira, Shujiro Inoue, et al.. (2002). Important Role of Rho-kinase in the Pathogenesis of Cardiovascular Inflammation and Remodeling Induced by Long-Term Blockade of Nitric Oxide Synthesis in Rats. Hypertension. 39(2). 245–250. 167 indexed citations
8.
Ikeda, Yasuhiro, Yoshikazu Yonemitsu, Chu Kataoka, et al.. (2002). Anti-monocyte chemoattractant protein-1 gene therapy attenuates pulmonary hypertension in rats. American Journal of Physiology-Heart and Circulatory Physiology. 283(5). H2021–H2028. 101 indexed citations
9.
Kataoka, Chu, et al.. (2001). Anti-monocyte chemoattractant protein-1 gene therapy inhibits restenotic changes after balloon angioplasty in hypercholesterolemic rabbits and monkeys. Circulation. 104(17). 146. 1 indexed citations
10.
Ni, Weihua, Kensuke Egashira, Chu Kataoka, et al.. (2001). Antiinflammatory and Antiarteriosclerotic Actions of HMG-CoA Reductase Inhibitors in a Rat Model of Chronic Inhibition of Nitric Oxide Synthesis. Circulation Research. 89(5). 415–421. 116 indexed citations
11.
Katoh, Makoto, Kensuke Egashira, Chu Kataoka, et al.. (2001). Regression by ACE inhibition of arteriosclerotic changes induced by chronic blockade of NO synthesis in rats. American Journal of Physiology-Heart and Circulatory Physiology. 280(5). H2306–H2312. 17 indexed citations
12.
Ni, Weihua, Kensuke Egashira, Shiro Kitamoto, et al.. (2001). New Anti–Monocyte Chemoattractant Protein-1 Gene Therapy Attenuates Atherosclerosis in Apolipoprotein E–Knockout Mice. Circulation. 103(16). 2096–2101. 205 indexed citations
14.
Kitamoto, Shiro, Kensuke Egashira, Chu Kataoka, et al.. (2000). Increased Activity of Nuclear Factor-κB Participates in Cardiovascular Remodeling Induced by Chronic Inhibition of Nitric Oxide Synthesis in Rats. Circulation. 102(7). 806–812. 72 indexed citations
16.
Kitamoto, Shiro, Kensuke Egashira, Chu Kataoka, et al.. (2000). Chronic inhibition of nitric oxide synthesis in rats increases aortic superoxide anion production via the action of angiotensin II. Journal of Hypertension. 18(12). 1795–1800. 58 indexed citations
17.
Usui, Makoto, Kensuke Egashira, Shiro Kitamoto, et al.. (1999). Pathogenic Role of Oxidative Stress in Vascular Angiotensin-Converting Enzyme Activation in Long-Term Blockade of Nitric Oxide Synthesis in Rats. Hypertension. 34(4). 546–551. 89 indexed citations

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.

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