Qinyu Ma

774 total citations
18 papers, 613 citations indexed

About

Qinyu Ma is a scholar working on Molecular Biology, Oncology and Orthopedics and Sports Medicine. According to data from OpenAlex, Qinyu Ma has authored 18 papers receiving a total of 613 indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Molecular Biology, 6 papers in Oncology and 4 papers in Orthopedics and Sports Medicine. Recurrent topics in Qinyu Ma's work include Bone Metabolism and Diseases (12 papers), Bone health and treatments (5 papers) and Extracellular vesicles in disease (5 papers). Qinyu Ma is often cited by papers focused on Bone Metabolism and Diseases (12 papers), Bone health and treatments (5 papers) and Extracellular vesicles in disease (5 papers). Qinyu Ma collaborates with scholars based in China and United States. Qinyu Ma's co-authors include Ce Dou, Mengmeng Liang, Fei Luo, Shiwu Dong, Jianzhong Xu, Ning Ding, Yun Bai, Fei Kang, Qijie Dai and Yutong Wu and has published in prestigious journals such as Journal of Biological Chemistry, Journal of Bone and Mineral Research and Journal of Cellular Physiology.

In The Last Decade

Qinyu Ma

18 papers receiving 609 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Qinyu Ma China 13 418 174 157 144 75 18 613
Abdul S. Qadir South Korea 15 509 1.2× 154 0.9× 127 0.8× 235 1.6× 90 1.2× 23 824
Feiwu Kang China 9 280 0.7× 126 0.7× 60 0.4× 137 1.0× 57 0.8× 27 499
Jasreen Kular Australia 10 480 1.1× 254 1.5× 71 0.5× 98 0.7× 121 1.6× 12 741
Masud Khan Japan 9 500 1.2× 271 1.6× 57 0.4× 148 1.0× 130 1.7× 14 683
Guochun Zhu United States 18 650 1.6× 252 1.4× 114 0.7× 195 1.4× 86 1.1× 25 882
Madoka Hayashi Japan 4 378 0.9× 210 1.2× 52 0.3× 91 0.6× 114 1.5× 7 507
Atsuhiro Fujie Japan 11 279 0.7× 124 0.7× 59 0.4× 97 0.7× 117 1.6× 16 495
Sylvia Thiele Germany 16 341 0.8× 182 1.0× 105 0.7× 63 0.4× 119 1.6× 23 598
Semun Seong South Korea 14 351 0.8× 123 0.7× 69 0.4× 118 0.8× 44 0.6× 32 489
Genki Kato Japan 4 333 0.8× 189 1.1× 46 0.3× 86 0.6× 96 1.3× 6 468

Countries citing papers authored by Qinyu Ma

Since Specialization
Citations

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

Fields of papers citing papers by Qinyu Ma

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Qinyu Ma

This figure shows the co-authorship network connecting the top 25 collaborators of Qinyu Ma. A scholar is included among the top collaborators of Qinyu Ma 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 Qinyu Ma. Qinyu Ma 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
1.
Wei, Xiaoyu, Mengmeng Liang, Min Deng, et al.. (2024). A switch from lysosomal degradation to secretory autophagy initiates osteogenic bone metastasis in prostate cancer. Journal of Extracellular Vesicles. 13(11). e70002–e70002. 3 indexed citations
2.
Zhang, Xiaoguang, Wei Chen, Shenghui Lan, et al.. (2023). Stem cell-derived small extracellular vesicles containing miR-27b-3p attenuated osteoarthritis through inhibition of leukaemia inhibitory factor. Fundamental Research. 5(4). 1804–1821. 2 indexed citations
3.
Liang, Mengmeng, Ke Wang, Xiaoyu Wei, et al.. (2023). Replenishing decoy extracellular vesicles inhibits phenotype remodeling of tissue-resident cells in inflammation-driven arthritis. Cell Reports Medicine. 4(10). 101228–101228. 9 indexed citations
4.
Wang, Ke, Mengmeng Liang, Yu Wang, et al.. (2022). Blockade of JAK2 retards cartilage degeneration and IL-6-induced pain amplification in osteoarthritis. International Immunopharmacology. 113. 109340–109340. 12 indexed citations
5.
6.
Liang, Mengmeng, Xiaofan Yin, Shuai Zhang, et al.. (2021). Osteoclast-derived small extracellular vesicles induce osteogenic differentiation via inhibiting ARHGAP1. Molecular Therapy — Nucleic Acids. 23. 1191–1203. 41 indexed citations
7.
Ma, Qinyu, Mengmeng Liang, Yutong Wu, et al.. (2021). Osteoclast-derived apoptotic bodies couple bone resorption and formation in bone remodeling. Bone Research. 9(1). 5–5. 73 indexed citations
8.
Li, Yang, Junxian Hu, Qinyu Ma, et al.. (2021). Light rare earth elements hinder bone development via inhibiting type H vessels formation in mice. Ecotoxicology and Environmental Safety. 218. 112275–112275. 9 indexed citations
9.
Ma, Qinyu, Mengmeng Liang, Yutong Wu, et al.. (2021). Small extracellular vesicles deliver osteolytic effectors and mediate cancer‐induced osteolysis in bone metastatic niche. Journal of Extracellular Vesicles. 10(4). e12068–e12068. 40 indexed citations
10.
Ma, Qinyu, Mengmeng Liang, Nathachit Limjunyawong, et al.. (2020). Osteoclast-derived apoptotic bodies show extended biological effects of parental cell in promoting bone defect healing. Theranostics. 10(15). 6825–6838. 54 indexed citations
11.
Ma, Qinyu, Mengmeng Liang, Yaxi Wang, et al.. (2020). Non‐coenzyme role of vitamin B1 in RANKL‐induced osteoclastogenesis and ovariectomy induced osteoporosis. Journal of Cellular Biochemistry. 121(7). 3526–3536. 13 indexed citations
12.
Ding, Ning, et al.. (2020). Physalin D inhibits RANKL-induced osteoclastogenesis and bone loss via regulating calcium signaling. BMB Reports. 53(3). 154–159. 13 indexed citations
13.
Ma, Qinyu, Mengmeng Liang, Yutong Wu, et al.. (2019). Mature osteoclast–derived apoptotic bodies promote osteogenic differentiation via RANKL-mediated reverse signaling. Journal of Biological Chemistry. 294(29). 11240–11247. 75 indexed citations
14.
Liang, Mengmeng, Qinyu Ma, Ning Ding, et al.. (2019). IL-11 is essential in promoting osteolysis in breast cancer bone metastasis via RANKL-independent activation of osteoclastogenesis. Cell Death and Disease. 10(5). 353–353. 76 indexed citations
15.
Ma, Qinyu, Mengmeng Liang, Fei Luo, et al.. (2019). The role of physical forces in osteoclastogenesis. Journal of Cellular Physiology. 234(8). 12498–12507. 15 indexed citations
16.
Ma, Qinyu, Mengmeng Liang, Xiangyu Tang, Fei Luo, & Ce Dou. (2019). Vitamin B5 inhibit RANKL induced osteoclastogenesis and ovariectomy induced osteoporosis by scavenging ROS generation.. PubMed. 11(8). 5008–5018. 23 indexed citations
17.
Ding, Ning, Chuan Liu, Yao Li, et al.. (2018). Alendronate induces osteoclast precursor apoptosis via peroxisomal dysfunction mediated ER stress. Journal of Cellular Physiology. 233(9). 7415–7423. 25 indexed citations
18.
Dou, Ce, Ning Ding, Chunrong Zhao, et al.. (2017). Estrogen Deficiency–Mediated M2 Macrophage Osteoclastogenesis Contributes to M1/M2 Ratio Alteration in Ovariectomized Osteoporotic Mice. Journal of Bone and Mineral Research. 33(5). 899–908. 128 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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