Shoujin Hao

518 total citations
29 papers, 442 citations indexed

About

Shoujin Hao is a scholar working on Molecular Biology, Physiology and Pulmonary and Respiratory Medicine. According to data from OpenAlex, Shoujin Hao has authored 29 papers receiving a total of 442 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Molecular Biology, 8 papers in Physiology and 6 papers in Pulmonary and Respiratory Medicine. Recurrent topics in Shoujin Hao's work include Ion Transport and Channel Regulation (8 papers), Electrolyte and hormonal disorders (6 papers) and Sodium Intake and Health (5 papers). Shoujin Hao is often cited by papers focused on Ion Transport and Channel Regulation (8 papers), Electrolyte and hormonal disorders (6 papers) and Sodium Intake and Health (5 papers). Shoujin Hao collaborates with scholars based in United States, Chile and Italy. Shoujin Hao's co-authors include Nicholas R. Ferreri, Paulina L. Pedraza, Charles T. Stier, Hong Zhao, Zbigniew Darżynkiewicz, Lars Bellner, Carlos P. Vío, John C. McGiff, Lesley Graham and Delyth Graham and has published in prestigious journals such as Journal of Biological Chemistry, The Journal of Physiology and The FASEB Journal.

In The Last Decade

Shoujin Hao

28 papers receiving 435 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Shoujin Hao United States 12 198 120 116 105 73 29 442
Trevor H. Thomas United Kingdom 14 198 1.0× 120 1.0× 48 0.4× 113 1.1× 113 1.5× 29 539
Shahla Riazi United States 14 334 1.7× 160 1.3× 119 1.0× 116 1.1× 280 3.8× 21 714
Henrik Andersen Denmark 12 146 0.7× 78 0.7× 70 0.6× 79 0.8× 55 0.8× 14 343
Sanket Patel United States 14 146 0.7× 68 0.6× 47 0.4× 51 0.5× 127 1.7× 35 505
Rob Barto Netherlands 15 156 0.8× 39 0.3× 64 0.6× 82 0.8× 134 1.8× 35 643
Megan E. Rudock United States 9 174 0.9× 22 0.2× 182 1.6× 89 0.8× 131 1.8× 10 572
Pablo Cabral United States 12 160 0.8× 30 0.3× 40 0.3× 76 0.7× 144 2.0× 23 435
Allison B. Lehtinen United States 13 158 0.8× 25 0.2× 57 0.5× 47 0.4× 106 1.5× 16 508
Nicolas Godin Canada 7 185 0.9× 25 0.2× 23 0.2× 122 1.2× 74 1.0× 8 437
Jean-François Thibodeau Canada 11 189 1.0× 43 0.4× 24 0.2× 172 1.6× 67 0.9× 21 454

Countries citing papers authored by Shoujin Hao

Since Specialization
Citations

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

Fields of papers citing papers by Shoujin Hao

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Shoujin Hao

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

All Works

20 of 20 papers shown
1.
Hao, Shoujin, et al.. (2025). TNF inhibits NKCC2 phosphorylation by a calcineurin-dependent pathway. American Journal of Physiology-Renal Physiology. 328(4). F489–F500.
2.
Hao, Shoujin, et al.. (2023). TNF inhibits AQP2 expression via a miR137-dependent pathway. Physiology. 38(S1). 1 indexed citations
3.
Hao, Shoujin, et al.. (2023). TNF inhibits AQP2 expression via a miR137-dependent pathway. American Journal of Physiology-Renal Physiology. 326(1). F152–F164. 3 indexed citations
5.
Drugge, Elizabeth, Shihua Zhao, Lesley Graham, et al.. (2022). Sex and race differences in urinary Tumor Necrosis Factor-α (TNF-α) levels: Secondary analysis of the DASH-sodium trial. Journal of Human Hypertension. 37(8). 701–708. 3 indexed citations
6.
Hao, Shoujin, et al.. (2022). MicroRNA-195a-5p Regulates Blood Pressure by Inhibiting NKCC2A. Hypertension. 80(2). 426–439. 8 indexed citations
7.
Hao, Shoujin, et al.. (2020). Effects of intron conversion in the human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice. Journal of Biological Chemistry. 295(32). 11068–11081. 2 indexed citations
8.
Hao, Shoujin, et al.. (2020). MicroRNA-133a-Dependent Inhibition of Proximal Tubule Angiotensinogen by Renal TNF (Tumor Necrosis Factor). Hypertension. 76(6). 1744–1752. 12 indexed citations
9.
Hao, Shoujin, et al.. (2019). Regulation of NKCC2B by TNF-α in response to salt restriction. American Journal of Physiology-Renal Physiology. 318(1). F273–F282. 9 indexed citations
11.
Hao, Shoujin, et al.. (2016). The EP3 receptor regulates water excretion in response to high salt intake. American Journal of Physiology-Renal Physiology. 311(4). F822–F829. 8 indexed citations
12.
Minuz, Pietro, Cristiano Fava, Shoujin Hao, et al.. (2014). Differential regulation of TNF receptors in maternal leukocytes is associated with severe preterm preeclampsia. The Journal of Maternal-Fetal & Neonatal Medicine. 28(8). 869–875. 8 indexed citations
13.
Vattemi, Gaetano, Matteo Marini, Nicholas R. Ferreri, et al.. (2013). Overexpression of TNF-α in mitochondrial diseases caused by mutations in mtDNA: evidence for signaling through its receptors on mitochondria. Free Radical Biology and Medicine. 63. 108–114. 9 indexed citations
14.
Hao, Shoujin, et al.. (2012). Tumor necrosis factor-alpha induces renal cyclooxygenase-2 expression in response to hypercalcemia. Prostaglandins & Other Lipid Mediators. 99(1-2). 45–50. 6 indexed citations
15.
Ferreri, Nicholas R., Shoujin Hao, Paulina L. Pedraza, Bruno Escalante, & Carlos P. Vío. (2011). Eicosanoids and tumor necrosis factor-alpha in the kidney. Prostaglandins & Other Lipid Mediators. 98(3-4). 101–106. 10 indexed citations
16.
Hao, Shoujin, et al.. (2011). Tumor necrosis factor-α is an endogenous inhibitor of Na+-K+-2Cl cotransporter (NKCC2) isoform A in the thick ascending limb. American Journal of Physiology-Renal Physiology. 301(1). F94–F100. 38 indexed citations
17.
Pedraza, Paulina L., et al.. (2010). TNFR1-deficient mice display altered blood pressure and renal responses to ANG II infusion. American Journal of Physiology-Renal Physiology. 299(5). F1141–F1150. 42 indexed citations
18.
Hao, Shoujin, et al.. (2009). Expression and function of NFAT5 in medullary thick ascending limb (mTAL) cells. American Journal of Physiology-Renal Physiology. 296(6). F1494–F1503. 21 indexed citations
19.
Mukhopadhyay, Somshuvra, Carlos P. Vío, Paulina L. Pedraza, et al.. (2007). Characterization of a long-term rat mTAL cell line. American Journal of Physiology-Renal Physiology. 293(4). F1413–F1422. 22 indexed citations
20.
Pedraza, Paulina L., et al.. (2005). NFAT regulates calcium-sensing receptor-mediated TNF production. American Journal of Physiology-Renal Physiology. 290(5). F1110–F1117. 33 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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