Y Yazaki

530 total citations
11 papers, 449 citations indexed

About

Y Yazaki is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine and Cancer Research. According to data from OpenAlex, Y Yazaki has authored 11 papers receiving a total of 449 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Molecular Biology, 6 papers in Cardiology and Cardiovascular Medicine and 2 papers in Cancer Research. Recurrent topics in Y Yazaki's work include Cardiac Fibrosis and Remodeling (3 papers), Cancer, Lipids, and Metabolism (2 papers) and Cardiomyopathy and Myosin Studies (2 papers). Y Yazaki is often cited by papers focused on Cardiac Fibrosis and Remodeling (3 papers), Cancer, Lipids, and Metabolism (2 papers) and Cardiomyopathy and Myosin Studies (2 papers). Y Yazaki collaborates with scholars based in Japan and Netherlands. Y Yazaki's co-authors include Masako Shimada, Tsutomu Yamazaki, Issei Komuro, Kenji Harada, S Ishibashi, Hisanaga Yagyu, Kenichi Ohashi, N Yamada, Takanari Gotoda and Chikafusa Fukazawa and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Biochemical and Biophysical Research Communications and European Heart Journal.

In The Last Decade

Y Yazaki

11 papers receiving 431 citations

Peers

Y Yazaki
C T Chan United States
C. Copin France
André van der Zee Netherlands
Fayanne E. Thorngate United States
Reiling Peng United States
Stela Z. Berisha United States
Y Yazaki
Citations per year, relative to Y Yazaki Y Yazaki (= 1×) peers Mireille Challah

Countries citing papers authored by Y Yazaki

Since Specialization
Citations

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

Fields of papers citing papers by Y Yazaki

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Y Yazaki

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

All Works

11 of 11 papers shown
1.
Yamazaki, Tsutomu & Y Yazaki. (2000). Molecular basis of cardiac hypertrophy. Zeitschrift für Kardiologie. 89(1). 1–6. 47 indexed citations
2.
Aikawa, Ryuichi, et al.. (2000). Rho plays an important role in angiotensin II-induced hypertrophic responses in cardiac myocytes. PubMed. 212(1-2). 177–182. 41 indexed citations
3.
Suzuki, Hiroshi, Yukiko Kurihara, Motohiro Takeya, et al.. (1997). The Multiple Roles of Macrophage Scavenger Receptors (MSR) in vivo : Resistance to Atherosclerosis and Susceptibility to Infection in MSR Knockout Mice. Journal of Atherosclerosis and Thrombosis. 4(1). 1–11. 45 indexed citations
4.
Osuga, Jun-ichi, Hiroaki Yagyu, Ken Ohashi, et al.. (1997). Effects of apo E Deficiency on Plasma Lipid Levels in Mice Lacking APOBEC-1. Biochemical and Biophysical Research Communications. 236(2). 375–378. 5 indexed citations
5.
Komuro, Issei, Yukio Hiroi, Ryuichi Aikawa, et al.. (1997). Autoregulation of human cardiac homeobox gene CSX1: mediation by the enhancer element in the first intron.. PubMed. Suppl 12. 10–4. 8 indexed citations
6.
Shimada, Masako, S Ishibashi, Hisanaga Yagyu, et al.. (1996). Suppression of diet-induced atherosclerosis in low density lipoprotein receptor knockout mice overexpressing lipoprotein lipase.. Proceedings of the National Academy of Sciences. 93(14). 7242–7246. 133 indexed citations
7.
Katoh, Yoshiko, Ichiro Shiojima, Kazuyuki Tobe, et al.. (1995). Protein kinase cascade activated by mechanical stress in cardiocytes: possible involvement of angiotensin II. European Heart Journal. 16(suppl C). 8–11. 13 indexed citations
8.
Yamazaki, Tsutomu, et al.. (1995). Interaction of cardiac myocytes and non-myocytes in mechanical stress-induced hypertrophy.. PubMed. 20(2). 109–17. 13 indexed citations
9.
Shimano, Hitoshi, Nobuhiro Yamada, Motoya Katsuki, et al.. (1992). Overexpression of apolipoprotein E in transgenic mice: marked reduction in plasma lipoproteins except high density lipoprotein and resistance against diet-induced hypercholesterolemia.. Proceedings of the National Academy of Sciences. 89(5). 1750–1754. 122 indexed citations
10.
Shimano, Hitoshi, Chikafusa Fukazawa, Yoshikazu Shibasaki, et al.. (1991). The effect of apo E secretion on lipoprotein uptake in transfected cells. Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism. 1086(3). 245–254. 17 indexed citations
11.
Komuro, Issei & Y Yazaki. (1987). [Mechanisms of myocardial hypertrophy].. PubMed. 35(7). 695–702. 5 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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