Guang‐Feng Zuo

564 total citations
26 papers, 391 citations indexed

About

Guang‐Feng Zuo is a scholar working on Cardiology and Cardiovascular Medicine, Molecular Biology and Surgery. According to data from OpenAlex, Guang‐Feng Zuo has authored 26 papers receiving a total of 391 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Cardiology and Cardiovascular Medicine, 11 papers in Molecular Biology and 8 papers in Surgery. Recurrent topics in Guang‐Feng Zuo's work include Coronary Interventions and Diagnostics (6 papers), Atherosclerosis and Cardiovascular Diseases (5 papers) and Angiogenesis and VEGF in Cancer (4 papers). Guang‐Feng Zuo is often cited by papers focused on Coronary Interventions and Diagnostics (6 papers), Atherosclerosis and Cardiovascular Diseases (5 papers) and Angiogenesis and VEGF in Cancer (4 papers). Guang‐Feng Zuo collaborates with scholars based in China, United States and Slovakia. Guang‐Feng Zuo's co-authors include Junjie Zhang, Shao‐Liang Chen, Xiaofei Gao, Zhimei Wang, Shao‐Liang Chen, Xiao‐Min Ren, Jie Luo, Peng Ye, Xiangquan Kong and Yue Gu and has published in prestigious journals such as SHILAP Revista de lepidopterología, PLoS ONE and The FASEB Journal.

In The Last Decade

Guang‐Feng Zuo

24 papers receiving 386 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Guang‐Feng Zuo China 12 161 148 90 65 43 26 391
Mingqi Zheng China 11 242 1.5× 161 1.1× 67 0.7× 31 0.5× 57 1.3× 63 472
Dajun Chai China 12 208 1.3× 80 0.5× 68 0.8× 70 1.1× 33 0.8× 32 423
Qiongfeng Wu China 13 206 1.3× 312 2.1× 63 0.7× 72 1.1× 40 0.9× 19 567
Kyle T. Keyes United States 7 206 1.3× 102 0.7× 80 0.9× 47 0.7× 82 1.9× 7 492
János Palóczi Hungary 14 194 1.2× 118 0.8× 63 0.7× 41 0.6× 92 2.1× 21 467
Xiao‐Min Ren China 9 113 0.7× 160 1.1× 101 1.1× 32 0.5× 21 0.5× 12 337
Anne-Marie Marés France 12 102 0.6× 115 0.8× 70 0.8× 65 1.0× 34 0.8× 15 460
Ben He China 11 156 1.0× 95 0.6× 83 0.9× 91 1.4× 61 1.4× 28 465
Masaaki Iwabayashi Japan 11 179 1.1× 100 0.7× 82 0.9× 41 0.6× 44 1.0× 24 442
Loubina Fazal France 11 347 2.2× 244 1.6× 102 1.1× 105 1.6× 41 1.0× 17 650

Countries citing papers authored by Guang‐Feng Zuo

Since Specialization
Citations

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

Fields of papers citing papers by Guang‐Feng Zuo

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Guang‐Feng Zuo. 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 Guang‐Feng Zuo. The network helps show where Guang‐Feng Zuo may publish in the future.

Co-authorship network of co-authors of Guang‐Feng Zuo

This figure shows the co-authorship network connecting the top 25 collaborators of Guang‐Feng Zuo. A scholar is included among the top collaborators of Guang‐Feng Zuo 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 Guang‐Feng Zuo. Guang‐Feng Zuo 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.
Wang, Feng, S Wang, Yue Gu, et al.. (2025). Disturbed shear stress promotes atherosclerosis through TRIM21‐regulated MAPK6 degradation and consequent endothelial inflammation. Clinical and Translational Medicine. 15(1). e70168–e70168. 2 indexed citations
2.
Gao, Xiaofei, Zhen Ge, Xiangquan Kong, et al.. (2024). Intravascular Ultrasound vs Angiography-Guided Drug-Coated Balloon Angioplasty. JACC: Cardiovascular Interventions. 17(13). 1519–1528. 17 indexed citations
3.
Zuo, Guang‐Feng, et al.. (2024). Prognostic value of serum angiopoietin-like protein 2 in patients with acute coronary syndrome. BMC Cardiovascular Disorders. 24(1). 709–709.
4.
Zuo, Guang‐Feng, Liguo Wang, Yifei Ren, et al.. (2023). TAX1BP1 downregulation by STAT3 in cardiac fibroblasts contributes to diabetes-induced heart failure with preserved ejection fraction. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1870(2). 166979–166979. 2 indexed citations
5.
Kong, Xiangquan, Liguo Wang, Feng Wang, et al.. (2022). Shear‐Induced ITGB4 Promotes Endothelial Cell Inflammation and Atherosclerosis. Oxidative Medicine and Cellular Longevity. 2022(1). 5842677–5842677. 7 indexed citations
6.
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Jiang, Xiaoxin, Yanrong Zhu, Zhicheng Wang, et al.. (2022). Targeting the KCa3.1 channel suppresses diabetes-associated atherosclerosis via the STAT3/CD36 axis. Diabetes Research and Clinical Practice. 185. 109776–109776. 7 indexed citations
8.
Gao, Xiaofei, Zhimei Wang, Feng Wang, et al.. (2021). Plasma Small Extracellular Vesicle‐Carried miRNA‐501‐5p Promotes Vascular Smooth Muscle Cell Phenotypic Modulation‐Mediated In‐Stent Restenosis. Oxidative Medicine and Cellular Longevity. 2021(1). 6644970–6644970. 11 indexed citations
9.
Gao, Xiaofei, Zhimei Wang, Feng Wang, et al.. (2021). Single-Cell RNA Sequencing of the Rat Carotid Arteries Uncovers Potential Cellular Targets of Neointimal Hyperplasia. Frontiers in Cardiovascular Medicine. 8. 751525–751525. 11 indexed citations
10.
Zuo, Guang‐Feng, Xiao‐Min Ren, Jie Luo, et al.. (2019). Activation of the PP2A catalytic subunit by ivabradine attenuates the development of diabetic cardiomyopathy. Journal of Molecular and Cellular Cardiology. 130. 170–183. 10 indexed citations
11.
12.
Zuo, Guang‐Feng, Xiao‐Min Ren, Xuesong Qian, et al.. (2018). Inhibition of JNK and p38 MAPK‐mediated inflammation and apoptosis by ivabradine improves cardiac function in streptozotocin‐induced diabetic cardiomyopathy. Journal of Cellular Physiology. 234(2). 1925–1936. 79 indexed citations
13.
Ye, Peng, Yue Gu, Yanrong Zhu, et al.. (2018). Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway. Journal of Cellular Physiology. 233(12). 9786–9798. 32 indexed citations
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Ren, Xiao‐Min, Guang‐Feng Zuo, Jie Luo, et al.. (2016). Atorvastatin Alleviates Experimental Diabetic Cardiomyopathy by Regulating the GSK-3β-PP2Ac-NF-κB Signaling Axis. PLoS ONE. 11(11). e0166740–e0166740. 26 indexed citations
18.
Zhang, Junxia, Zhimei Wang, Junjie Zhang, et al.. (2014). Rapamycin Attenuates Endothelial Apoptosis Induced by Low Shear Stress via mTOR and Sestrin1 Related Redox Regulation. Mediators of Inflammation. 2014. 1–9. 30 indexed citations
19.
Chen, Shao‐Liang, Zuo‐Ying Hu, Guang‐Feng Zuo, Minghui Li, & Bin Li. (2014). I(f) current channel inhibitor (ivabradine) deserves cardioprotective effect via down-regulating the expression of matrix metalloproteinase (MMP)-2 and attenuating apoptosis in diabetic mice. BMC Cardiovascular Disorders. 14(1). 150–150. 21 indexed citations
20.
Zhang, Junxia, Zhimei Wang, Guang‐Feng Zuo, et al.. (2013). Low shear stress induces human vascular endothelial cell apoptosis by activating Akt signal and increasing reactive oxygen species.. PubMed. 33(3). 313–7. 17 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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