Bonnie Eby

1.1k total citations · 1 hit paper
18 papers, 883 citations indexed

About

Bonnie Eby is a scholar working on Molecular Biology, Nephrology and Endocrinology, Diabetes and Metabolism. According to data from OpenAlex, Bonnie Eby has authored 18 papers receiving a total of 883 indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 9 papers in Nephrology and 4 papers in Endocrinology, Diabetes and Metabolism. Recurrent topics in Bonnie Eby's work include Parathyroid Disorders and Treatments (7 papers), Ion Transport and Channel Regulation (4 papers) and Renal function and acid-base balance (3 papers). Bonnie Eby is often cited by papers focused on Parathyroid Disorders and Treatments (7 papers), Ion Transport and Channel Regulation (4 papers) and Renal function and acid-base balance (3 papers). Bonnie Eby collaborates with scholars based in United States, Italy and United Kingdom. Bonnie Eby's co-authors include Kai Lau, Hongliang Li, David C. Kem, Yunzhou Dong, Ming-Hui Zou, Rong Tian, Chaoyong He, Shradha Rathi, Becky Pennington and Pedro Moreno and has published in prestigious journals such as Journal of Biological Chemistry, Journal of Clinical Investigation and Diabetes.

In The Last Decade

Bonnie Eby

17 papers receiving 835 citations

Hit Papers

Improvement of Cardiac Functions by Chronic Metformin Tre... 2011 2026 2016 2021 2011 100 200 300 400

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Bonnie Eby United States 13 357 214 175 170 149 18 883
Nobuyuki Banba Japan 18 246 0.7× 96 0.4× 129 0.7× 257 1.5× 248 1.7× 35 978
Mototaka Yoshinari Japan 21 235 0.7× 121 0.6× 126 0.7× 486 2.9× 147 1.0× 50 1.0k
Karine Demuth France 18 176 0.5× 86 0.4× 256 1.5× 83 0.5× 155 1.0× 26 1.1k
Masanori Iwase Japan 17 194 0.5× 164 0.8× 142 0.8× 261 1.5× 161 1.1× 45 815
Oana Sandu United States 10 304 0.9× 86 0.4× 167 1.0× 304 1.8× 323 2.2× 12 1.0k
Ann‐Christine Eklöf Sweden 16 376 1.1× 46 0.2× 85 0.5× 191 1.1× 92 0.6× 27 986
Ashley Pitzer United States 13 485 1.4× 167 0.8× 125 0.7× 105 0.6× 140 0.9× 23 910
M. Schumer United States 9 252 0.7× 48 0.2× 113 0.6× 101 0.6× 269 1.8× 12 995
Hideaki Nakatsuji Japan 19 400 1.1× 376 1.8× 187 1.1× 153 0.9× 221 1.5× 37 1.1k
Sung Woo Ha South Korea 9 169 0.5× 119 0.6× 185 1.1× 186 1.1× 354 2.4× 19 945

Countries citing papers authored by Bonnie Eby

Since Specialization
Citations

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

Fields of papers citing papers by Bonnie Eby

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Bonnie Eby

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

All Works

18 of 18 papers shown
2.
Eby, Bonnie, Vasyl Nesin, Megan R. Lerner, et al.. (2020). Control of PTH secretion by the TRPC1 ion channel. JCI Insight. 5(8). 9 indexed citations
3.
Khan, Usman A., et al.. (2020). Induction of CKD by Gene Deletion of Canonical Transient Receptor Potential 1 (TRPC1) Channels Independent of Hypertension and Nephromegaly Despite Diabetes and Metabolic Syndrome. Journal of the American Society of Nephrology. 31(10S). 231–231. 1 indexed citations
4.
He, Xuemin, Rui Cheng, Kyoungmin Park, et al.. (2016). Pigment epithelium-derived factor, a noninhibitory serine protease inhibitor, is renoprotective by inhibiting the Wnt pathway. Kidney International. 91(3). 642–657. 27 indexed citations
5.
Xie, Zhonglin, Kai Lau, Bonnie Eby, et al.. (2011). Improvement of Cardiac Functions by Chronic Metformin Treatment Is Associated With Enhanced Cardiac Autophagy in Diabetic OVE26 Mice. Diabetes. 60(6). 1770–1778. 423 indexed citations breakdown →
6.
Lau, Kai, Daren McCalla, Bonnie Eby, et al.. (2010). Deletion of the Receptor for Advanced Glycation End Products Reduces Glomerulosclerosis and Preserves Renal Function in the Diabetic OVE26 Mouse. Diabetes. 59(8). 2043–2054. 142 indexed citations
7.
Bourdeau, J. E. & Bonnie Eby. (1990). cAMP-stimulated rise of [Ca2+]i in rabbit connecting tubules: role of peritubular Ca. American Journal of Physiology-Renal Physiology. 258(3). F751–F755. 16 indexed citations
8.
Lau, Kai, Debby Thomas, & Bonnie Eby. (1986). The nature and role of disturbances in calcium metabolism in genetic hypertension.. PubMed. 45(12). 2752–7. 4 indexed citations
9.
Brasitus, Thomas A., Pradeep K. Dudeja, Bonnie Eby, & Kai Lau. (1986). Correction by 1-25-dihydroxycholecalciferol of the abnormal fluidity and lipid composition of enterocyte brush border membranes in vitamin D-deprived rats.. Journal of Biological Chemistry. 261(35). 16404–16409. 46 indexed citations
10.
Lau, Kai, et al.. (1986). Evidence against the role of calcium deficiency in genetic hypertension.. Hypertension. 8(1). 45–49. 17 indexed citations
11.
Gafter, Uzi, Bonnie Eby, Craig A. Martin, & Kai Lau. (1986). Response of spontaneously hypertensive rats to 1,25(OH)2D3 in vivo. Kidney International. 30(4). 497–502. 3 indexed citations
12.
Lau, Kai, Debby Thomas, Craig B. Langman, & Bonnie Eby. (1985). Pathophysiology of spontaneous hypercalciuria in laboratory rats. Role of deranged vitamin D metabolism.. Journal of Clinical Investigation. 76(2). 420–425. 12 indexed citations
13.
Lau, Kai & Bonnie Eby. (1985). The role of calcium in genetic hypertension.. Hypertension. 7(5). 657–667. 48 indexed citations
14.
Lau, Kai, et al.. (1984). Evidence for the role of PO4 deficiency in antihypertensive action of a high-Ca diet. American Journal of Physiology-Heart and Circulatory Physiology. 246(3). H324–H331. 42 indexed citations
15.
Lau, Kai, et al.. (1984). Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats. American Journal of Physiology-Endocrinology and Metabolism. 247(5). E625–E633. 35 indexed citations
16.
Lau, Kai, J. Guntupalli, & Bonnie Eby. (1983). Effects of somatostatin on phosphate transport: Evidence for the role of basal insulin. Kidney International. 24(1). 10–15. 16 indexed citations
17.
Lau, Kai & Bonnie Eby. (1982). Tubular Mechanism for the Spontaneous Hypercalciuria in Laboratory Rat. Journal of Clinical Investigation. 70(4). 835–844. 15 indexed citations
18.
Guntupalli, J., Bonnie Eby, & Kai Lau. (1982). Mechanism for the phosphaturia of NH4Cl: dependence on acidemia but not on diet PO4 or PTH. American Journal of Physiology-Renal Physiology. 242(5). F552–F560. 27 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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