Mingge Ding

1.6k total citations
21 papers, 1.2k citations indexed

About

Mingge Ding is a scholar working on Molecular Biology, Cardiology and Cardiovascular Medicine and Pathology and Forensic Medicine. According to data from OpenAlex, Mingge Ding has authored 21 papers receiving a total of 1.2k indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Molecular Biology, 10 papers in Cardiology and Cardiovascular Medicine and 6 papers in Pathology and Forensic Medicine. Recurrent topics in Mingge Ding's work include Mitochondrial Function and Pathology (12 papers), ATP Synthase and ATPases Research (6 papers) and Cardiac Ischemia and Reperfusion (6 papers). Mingge Ding is often cited by papers focused on Mitochondrial Function and Pathology (12 papers), ATP Synthase and ATPases Research (6 papers) and Cardiac Ischemia and Reperfusion (6 papers). Mingge Ding collaborates with scholars based in China, United States and Russia. Mingge Ding's co-authors include Feng Fu, Xiaoming Gu, Na Feng, Zhenhua Liu, Xiaoming Wang, Min Jia, Yuemin Wang, Zeyang Li, Jiahao Feng and Rui Shi and has published in prestigious journals such as SHILAP Revista de lepidopterología, Biochemical and Biophysical Research Communications and Antioxidants and Redox Signaling.

In The Last Decade

Mingge Ding

20 papers receiving 1.2k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Mingge Ding China 13 714 280 245 190 154 21 1.2k
Haifeng Pei China 18 532 0.7× 212 0.8× 324 1.3× 158 0.8× 152 1.0× 52 1.2k
Xiaodong Xue China 20 627 0.9× 310 1.1× 230 0.9× 162 0.9× 180 1.2× 46 1.4k
Nathan D. Roe United States 14 629 0.9× 382 1.4× 383 1.6× 197 1.0× 95 0.6× 18 1.2k
Fanghao Lu China 25 545 0.8× 244 0.9× 294 1.2× 193 1.0× 177 1.1× 39 1.2k
Yuichiro Mita Japan 15 563 0.8× 152 0.5× 215 0.9× 390 2.1× 104 0.7× 24 1.2k
Emilie Vessières France 21 546 0.8× 273 1.0× 337 1.4× 112 0.6× 75 0.5× 46 1.3k
Natasha Fillmore United States 20 926 1.3× 480 1.7× 554 2.3× 222 1.2× 110 0.7× 32 1.6k
Yinli Xu China 15 488 0.7× 206 0.7× 200 0.8× 109 0.6× 122 0.8× 34 953

Countries citing papers authored by Mingge Ding

Since Specialization
Citations

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

Fields of papers citing papers by Mingge Ding

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Mingge Ding

This figure shows the co-authorship network connecting the top 25 collaborators of Mingge Ding. A scholar is included among the top collaborators of Mingge Ding 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 Mingge Ding. Mingge Ding 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.
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Shi, Rui, Zhenhua Liu, Huan Yue, et al.. (2024). IP3R1-mediated MAMs formation contributes to mechanical trauma-induced hepatic injury and the protective effect of melatonin. Cellular & Molecular Biology Letters. 29(1). 22–22. 5 indexed citations
3.
Gao, Tian, Rui Shi, Zhenhua Liu, et al.. (2023). Ischemia/reperfusion-induced MiD51 upregulation recruits Drp1 to mitochondria and contributes to myocardial injury. Biochemical and Biophysical Research Communications. 665. 78–87. 3 indexed citations
4.
Ding, Mingge, Rui Shi, Feng Fu, et al.. (2022). Paeonol protects against doxorubicin-induced cardiotoxicity by promoting Mfn2-mediated mitochondrial fusion through activating the PKCε-Stat3 pathway. Journal of Advanced Research. 47. 151–162. 49 indexed citations
5.
Ding, Mingge, Rui Shi, Man Li, et al.. (2022). Mfn2-mediated mitochondrial fusion alleviates doxorubicin-induced cardiotoxicity with enhancing its anticancer activity through metabolic switch. Redox Biology. 52. 102311–102311. 69 indexed citations
6.
Liu, Chaoyang, Yuehu Han, Xiaoming Gu, et al.. (2021). Paeonol promotes Opa1-mediated mitochondrial fusion via activating the CK2α-Stat3 pathway in diabetic cardiomyopathy. Redox Biology. 46. 102098–102098. 76 indexed citations
7.
Fu, Feng, Chaoyang Liu, Rui Shi, et al.. (2021). Punicalagin Protects Against Diabetic Cardiomyopathy by Promoting Opa1-Mediated Mitochondrial Fusion via Regulating PTP1B-Stat3 Pathway. Antioxidants and Redox Signaling. 35(8). 618–641. 23 indexed citations
8.
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10.
Ding, Mingge, Lang Hu, Hongyan Yang, et al.. (2019). Reduction of SIRT1 blunts the protective effects of ischemic post-conditioning in diabetic mice by impairing the Akt signaling pathway. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1865(6). 1677–1689. 9 indexed citations
11.
Hu, Lang, Mingge Ding, Erhe Gao, et al.. (2019). Targeting mitochondrial dynamics by regulating Mfn2 for therapeutic intervention in diabetic cardiomyopathy. Theranostics. 9(13). 3687–3706. 179 indexed citations
12.
Ding, Mingge, Chaoyang Liu, Rui Shi, et al.. (2019). Mitochondrial fusion promoter restores mitochondrial dynamics balance and ameliorates diabetic cardiomyopathy in an optic atrophy 1‐dependent way. Acta Physiologica. 229(1). e13428–e13428. 68 indexed citations
13.
Ding, Mingge, Na Feng, Jiahao Feng, et al.. (2018). Melatonin prevents D rp1‐mediated mitochondrial fission in diabetic hearts through SIRT 1‐ PGC 1α pathway. Journal of Pineal Research. 65(2). e12491–e12491. 304 indexed citations
14.
Ding, Mingge, Qianqian Dong, Zheng Liu, et al.. (2017). Inhibition of dynamin-related protein 1 protects against myocardial ischemia–reperfusion injury in diabetic mice. Cardiovascular Diabetology. 16(1). 19–19. 105 indexed citations
15.
Ding, Mingge, Yin Wang, Di Sun, et al.. (2017). Punicalagin Pretreatment Attenuates Myocardial Ischemia-Reperfusion Injury via Activation of AMPK. The American Journal of Chinese Medicine. 45(1). 53–66. 35 indexed citations
16.
Ding, Mingge, Na Feng, Zeyang Li, et al.. (2017). Dynamin‐related protein 1‐mediated mitochondrial fission contributes to post‐traumatic cardiac dysfunction in rats and the protective effect of melatonin. Journal of Pineal Research. 64(1). 81 indexed citations
17.
Ding, Mingge, Huan Zhang, Shuwen Liu, et al.. (2015). Calorie Restriction Attenuates Monocrotaline-induced Pulmonary Arterial Hypertension in Rats. Journal of Cardiovascular Pharmacology. 65(6). 562–570. 16 indexed citations
18.
Ding, Mingge, et al.. (2015). SIRT1 protects against myocardial ischemia–reperfusion injury via activating eNOS in diabetic rats. Cardiovascular Diabetology. 14(1). 143–143. 107 indexed citations
19.
Wang, Wenqing, Wenjuan Xing, Haifeng Zhang, et al.. (2012). Reduced high‐molecular‐weight adiponectin is an independent risk factor for cardiovascular lesions in hypercholesterolaemic patients. Clinical Endocrinology. 78(4). 539–544. 10 indexed citations
20.

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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