Tetsuya Nagae

954 total citations
10 papers, 822 citations indexed

About

Tetsuya Nagae is a scholar working on Molecular Biology, Nephrology and Endocrinology, Diabetes and Metabolism. According to data from OpenAlex, Tetsuya Nagae has authored 10 papers receiving a total of 822 indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Molecular Biology, 4 papers in Nephrology and 3 papers in Endocrinology, Diabetes and Metabolism. Recurrent topics in Tetsuya Nagae's work include Connective Tissue Growth Factor Research (3 papers), Receptor Mechanisms and Signaling (2 papers) and Neuropeptides and Animal Physiology (2 papers). Tetsuya Nagae is often cited by papers focused on Connective Tissue Growth Factor Research (3 papers), Receptor Mechanisms and Signaling (2 papers) and Neuropeptides and Animal Physiology (2 papers). Tetsuya Nagae collaborates with scholars based in Japan. Tetsuya Nagae's co-authors include Akira Sugawara, Masashi Mukoyama, Kiyoshi Mori, Takayoshi Suganami, Kazuwa Nakao, Hideki Yokoi, Tetsuro Yoshioka, Hisashi Makino, Kensei Yahata and Kazutomo Sawai and has published in prestigious journals such as Biochemical and Biophysical Research Communications, Journal of the American Society of Nephrology and American Journal of Physiology-Renal Physiology.

In The Last Decade

Tetsuya Nagae

10 papers receiving 812 citations

Peers

Tetsuya Nagae
Jeong Suk Kang South Korea
Tetsuya Nagae
Citations per year, relative to Tetsuya Nagae Tetsuya Nagae (= 1×) peers Jeong Suk Kang

Countries citing papers authored by Tetsuya Nagae

Since Specialization
Citations

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

Fields of papers citing papers by Tetsuya Nagae

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Tetsuya Nagae

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

All Works

10 of 10 papers shown
1.
Koshikawa, Masao, Masashi Mukoyama, Kiyoshi Mori, et al.. (2005). Role of p38 Mitogen-Activated Protein Kinase Activation in Podocyte Injury and Proteinuria in Experimental Nephrotic Syndrome. Journal of the American Society of Nephrology. 16(9). 2690–2701. 148 indexed citations
2.
Yokoi, Hideki, Masashi Mukoyama, Tetsuya Nagae, et al.. (2004). Reduction in Connective Tissue Growth Factor by Antisense Treatment Ameliorates Renal Tubulointerstitial Fibrosis. Journal of the American Society of Nephrology. 15(6). 1430–1440. 208 indexed citations
3.
Yahata, Kensei, Kiyoshi Mori, Masashi Mukoyama, et al.. (2003). Regulation of stanniocalcin 1 and 2 expression in the kidney by klotho gene. Biochemical and Biophysical Research Communications. 310(1). 128–134. 27 indexed citations
4.
Sawai, Kazutomo, Kiyoshi Mori, Masashi Mukoyama, et al.. (2003). Angiogenic Protein Cyr61 is Expressed by Podocytes in Anti-Thy-1 Glomerulonephritis. Journal of the American Society of Nephrology. 14(5). 1154–1163. 29 indexed citations
5.
Yokoi, Hideki, Masashi Mukoyama, Akira Sugawara, et al.. (2002). Role of connective tissue growth factor in fibronectin expression and tubulointerstitial fibrosis. American Journal of Physiology-Renal Physiology. 282(5). F933–F942. 146 indexed citations
6.
Suganami, Takayoshi, Masashi Mukoyama, Akira Sugawara, et al.. (2001). Overexpression of Brain Natriuretic Peptide in Mice Ameliorates Immune-Mediated Renal Injury. Journal of the American Society of Nephrology. 12(12). 2652–2663. 67 indexed citations
7.
Mukoyama, Masashi, Akira Sugawara, Tetsuya Nagae, et al.. (2001). Role of adrenomedullin and its receptor system in renal pathophysiology. Peptides. 22(11). 1925–1931. 15 indexed citations
8.
Nagae, Tetsuya, Masashi Mukoyama, Akira Sugawara, et al.. (2000). Rat Receptor-Activity-Modifying Proteins (RAMPs) for Adrenomedullin/CGRP Receptor: Cloning and Upregulation in Obstructive Nephropathy. Biochemical and Biophysical Research Communications. 270(1). 89–93. 98 indexed citations
9.
Mori, Kiyoshi, Kensei Yahata, Masashi Mukoyama, et al.. (2000). Disruption of klotho Gene Causes an Abnormal Energy Homeostasis in Mice. Biochemical and Biophysical Research Communications. 278(3). 665–670. 53 indexed citations
10.
Tanaka, Atsuo, Ritsuo Nishida, Kazutomo Sawai, et al.. (1997). [Traditional remedy-induced Chinese herbs nephropathy showing rapid deterioration of renal function].. PubMed. 39(8). 794–7. 31 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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