Sheng Jin

1.9k total citations
71 papers, 1.6k citations indexed

About

Sheng Jin is a scholar working on Biochemistry, Physiology and Endocrine and Autonomic Systems. According to data from OpenAlex, Sheng Jin has authored 71 papers receiving a total of 1.6k indexed citations (citations by other indexed papers that have themselves been cited), including 39 papers in Biochemistry, 24 papers in Physiology and 15 papers in Endocrine and Autonomic Systems. Recurrent topics in Sheng Jin's work include Sulfur Compounds in Biology (39 papers), Neuroscience of respiration and sleep (11 papers) and Nitric Oxide and Endothelin Effects (10 papers). Sheng Jin is often cited by papers focused on Sulfur Compounds in Biology (39 papers), Neuroscience of respiration and sleep (11 papers) and Nitric Oxide and Endothelin Effects (10 papers). Sheng Jin collaborates with scholars based in China, United States and South Korea. Sheng Jin's co-authors include Yuming Wu, Xu Teng, Qi Guo, Lin Xiao, Danyang Tian, Hongmei Xue, Yuhong Chen, Yi‐Chun Zhu, Ming-Jie Wang and Jinghui Dong and has published in prestigious journals such as PLoS ONE, Acta Materialia and Scientific Reports.

In The Last Decade

Sheng Jin

67 papers receiving 1.6k citations

Peers

Sheng Jin
Yusuf Ali Singapore
Ameya Kulkarni United States
Katalin Erdélyi United States
Chelsea L. Organ United States
David J. Polhemus United States
Yusuf Ali Singapore
Sheng Jin
Citations per year, relative to Sheng Jin Sheng Jin (= 1×) peers Yusuf Ali

Countries citing papers authored by Sheng Jin

Since Specialization
Citations

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

Fields of papers citing papers by Sheng Jin

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Sheng Jin

This figure shows the co-authorship network connecting the top 25 collaborators of Sheng Jin. A scholar is included among the top collaborators of Sheng Jin 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 Sheng Jin. Sheng Jin 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.
Jiao, Jie, Lisha Ma, Dongmei Li, et al.. (2025). Mitochondrial RNA/RIG-I promotes Caspase-1/GSDMD-mediated inflammation in sepsis-associated acute kidney injury. Immunobiology. 230(4). 153085–153085.
3.
Li, Yongqin, Jiawei Du, Ruiqian Li, et al.. (2024). The withdrawal time of enrofloxacin, sulfachloropyrazine sodium, and doxycycline as well as the in vitro binding interaction with melanin in black-feathered silky fowl. Food Chemistry X. 24. 101994–101994. 1 indexed citations
4.
Zhang, Qian, Da Liu, Xiaoyu Bai, et al.. (2024). PCSK9 promotes vascular neointimal hyperplasia through non-lipid regulation of vascular smooth muscle cell proliferation, migration, and autophagy. Biochemical and Biophysical Research Communications. 742. 151081–151081. 3 indexed citations
5.
Chen, Qian, Jiao Xu, Qi Guo, et al.. (2024). H2S alleviated sepsis-induced acute kidney injury by inhibiting PERK/Bax-Bcl2 pathway. Nitric Oxide. 152. 11–18. 3 indexed citations
6.
Zhang, Huaxing, Bo Tan, Lixia Zhang, et al.. (2024). Hydrogen Sulfide Ameliorates Heart Aging by Downregulating Matrix Metalloproteinase-9. Cardiovascular Drugs and Therapy. 39(5). 967–981. 3 indexed citations
7.
Jin, Sheng, et al.. (2023). Small-molecule BCL6 inhibitor protects chronic cardiac transplant rejection and inhibits T follicular helper cell expansion and humoral response. Frontiers in Pharmacology. 14. 1140703–1140703. 2 indexed citations
8.
Geng, Qi, et al.. (2023). Exercise protects vascular function by countering senescent cells in older adults. Frontiers in Physiology. 14. 1138162–1138162. 10 indexed citations
9.
Miao, Yi, et al.. (2023). Hydrogen Sulfide Alleviates Lipopolysaccharide-Induced Myocardial Injury Through TLR4-NLRP3 Pathway. Physiological Research. 72(1). 15–25. 8 indexed citations
10.
Guo, Qi, et al.. (2023). Melatonin suppresses sympathetic vasomotor tone through enhancing GABAA receptor activity in the hypothalamus. Frontiers in Physiology. 14. 1166246–1166246. 11 indexed citations
11.
Xue, Hongmei, Qi Guo, Danyang Tian, et al.. (2022). Hydrogen Sulfide Ameliorated High Choline‐Induced Cardiac Dysfunction by Inhibiting cGAS‐STING‐NLRP3 Inflammasome Pathway. Oxidative Medicine and Cellular Longevity. 2022(1). 1392896–1392896. 17 indexed citations
12.
Teng, Xu, et al.. (2021). The Antiviral Roles of Hydrogen Sulfide by Blocking the Interaction between SARS‐CoV‐2 and Its Potential Cell Surface Receptors. Oxidative Medicine and Cellular Longevity. 2021(1). 7866992–7866992. 18 indexed citations
13.
Zhang, Huaxing, Danyang Tian, Lin Xiao, et al.. (2021). Hydrogen Sulfide Restored the Diurnal Variation in Cardiac Function of Aging Mice. Oxidative Medicine and Cellular Longevity. 2021(1). 8841575–8841575. 13 indexed citations
14.
Teng, Xu, Hui Li, Hongmei Xue, et al.. (2019). GABAA receptor, KATP channel and L-type Ca2+ channel is associated with facilitation effect of H2S on the baroreceptor reflex in spontaneous hypertensive rats. Pharmacological Reports. 71(5). 968–975. 10 indexed citations
15.
Chen, Yuhong, Sheng Jin, Xu Teng, et al.. (2018). Hydrogen Sulfide Attenuates LPS‐Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative Stress. Oxidative Medicine and Cellular Longevity. 2018(1). 6717212–6717212. 145 indexed citations
16.
Yang, Yurong, Ge Lin, Youping Wang, et al.. (2018). Hydrogen Sulfide Alleviates Acute Myocardial Ischemia Injury by Modulating Autophagy and Inflammation Response under Oxidative Stress. Oxidative Medicine and Cellular Longevity. 2018(1). 3402809–3402809. 34 indexed citations
17.
Xiao, Lin, Jinghui Dong, Xu Teng, et al.. (2017). Hydrogen sulfide improves endothelial dysfunction in hypertension by activating peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase signaling. Journal of Hypertension. 36(3). 651–665. 51 indexed citations
18.
Xiao, Lin, Jinghui Dong, Sheng Jin, et al.. (2016). Hydrogen Sulfide Improves Endothelial Dysfunction via Downregulating BMP4/COX‐2 Pathway in Rats with Hypertension. Oxidative Medicine and Cellular Longevity. 2016(1). 8128957–8128957. 49 indexed citations
19.
Li, Na, Ming-Jie Wang, Sheng Jin, et al.. (2016). The H2S Donor NaHS Changes the Expression Pattern of H2S‐Producing Enzymes after Myocardial Infarction. Oxidative Medicine and Cellular Longevity. 2016(1). 6492469–6492469. 44 indexed citations
20.
Liu, Shangyu, Rong Guo, Lin Xiao, et al.. (2015). Cystathionine-β-Synthase Gene Transfer Into Rostral Ventrolateral Medulla Exacerbates Hypertension via Nitric Oxide in Spontaneously Hypertensive Rats. American Journal of Hypertension. 28(9). 1106–1113. 23 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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