Die Pu

506 total citations
10 papers, 405 citations indexed

About

Die Pu is a scholar working on Molecular Biology, Physiology and Neurology. According to data from OpenAlex, Die Pu has authored 10 papers receiving a total of 405 indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Molecular Biology, 4 papers in Physiology and 3 papers in Neurology. Recurrent topics in Die Pu's work include Muscle Physiology and Disorders (3 papers), Neuroinflammation and Neurodegeneration Mechanisms (3 papers) and Neurological Disease Mechanisms and Treatments (2 papers). Die Pu is often cited by papers focused on Muscle Physiology and Disorders (3 papers), Neuroinflammation and Neurodegeneration Mechanisms (3 papers) and Neurological Disease Mechanisms and Treatments (2 papers). Die Pu collaborates with scholars based in China. Die Pu's co-authors include Qian Xiao, Yuxing Zhao, Kexiang Zhao, Jinliang Chen, Cheng Luo, Zhiyin Liao, Shiyu Zhu, Yue Sun, Jing Zhou and Yue Sun and has published in prestigious journals such as Neuroscience, Experimental Cell Research and Life Sciences.

In The Last Decade

Die Pu

10 papers receiving 402 citations

Peers

Die Pu

MB

PHYSI

NEURO

EPIDE

EDM

Lihua Qian China

Matthew Wai Kin Wong Australia

Fengwei Nan China

Cheng Luo China

Chang-Nan Wang China

Chin‐ok Yi South Korea

Sylwia Wójtowicz Poland

Dalia M. El-Tanbouly Egypt

Yuyan Zhu United States

Lihua Qian China

Die Pu

181 ×0.9

MB

166 ×0.9

PHYSI

70 ×1.1

NEURO

56 ×0.9

EPIDE

55 ×1.5

EDM

Citations per year, relative to Die Pu Die Pu (= 1×) peers Lihua Qian

Countries citing papers authored by Die Pu

Since Specialization

Citations

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

Fields of papers citing papers by Die Pu

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Die Pu

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

All Works

Sort: Min cites: Since: Top N: Style:

10 of 10 papers shown

1.

Wang, Meili, Die Pu, Yuxing Zhao, et al.. (2020). Sulforaphane protects against skeletal muscle dysfunction in spontaneous type 2 diabetic db/db mice. Life Sciences. 255. 117823–117823. 29 indexed citations

2.

Zhu, Shiyu, Ankang Lü, Yuxing Zhao, et al.. (2020). [Expressions of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinases 1 in skeletal muscles of aged rats with sarcopenia].. PubMed. 40(1). 104–109. 1 indexed citations

3.

Zhu, Shiyu, Jinliang Chen, Yuxing Zhao, et al.. (2019). Inhibition of TLR9 attenuates skeletal muscle fibrosis in aged sarcopenic mice via the p53/SIRT1 pathway. Experimental Gerontology. 122. 25–33. 26 indexed citations

4.

Pu, Die, Yuxing Zhao, Jinliang Chen, et al.. (2018). Protective Effects of Sulforaphane on Cognitive Impairments and AD-like Lesions in Diabetic Mice are Associated with the Upregulation of Nrf2 Transcription Activity. Neuroscience. 381. 35–45. 57 indexed citations

5.

Chen, Jinliang, Cheng Luo, Die Pu, et al.. (2018). Metformin attenuates diabetes-induced tau hyperphosphorylation in vitro and in vivo by enhancing autophagic clearance. Experimental Neurology. 311. 44–56. 99 indexed citations

6.

Zhao, Yuxing, Cheng Luo, Jinliang Chen, et al.. (2018). High glucose‐induced complement component 3 up‐regulation via RAGE‐p38MAPK‐NF‐κB signalling in astrocytes: In vivo and in vitro studies. Journal of Cellular and Molecular Medicine. 22(12). 6087–6098. 26 indexed citations

7.

Chen, Jinliang, Dongling Zhang, Yue Sun, et al.. (2017). Angiotensin-(1–7) administration attenuates Alzheimer’s disease-like neuropathology in rats with streptozotocin-induced diabetes via Mas receptor activation. Neuroscience. 346. 267–277. 39 indexed citations

8.

Sun, Yue, Qian Xiao, Cheng Luo, et al.. (2017). High-glucose induces tau hyperphosphorylation through activation of TLR9-P38MAPK pathway. Experimental Cell Research. 359(2). 312–318. 33 indexed citations

9.

Zhao, Yuxing, Die Pu, Yue Sun, et al.. (2017). High glucose-induced defective thrombospondin-1 release from astrocytes via TLR9 activation contributes to the synaptic protein loss. Experimental Cell Research. 363(2). 171–178. 13 indexed citations

10.

Liao, Zhiyin, Jinliang Chen, Yue Sun, et al.. (2017). The effect of exercise, resveratrol or their combination on Sarcopenia in aged rats via regulation of AMPK/Sirt1 pathway. Experimental Gerontology. 98. 177–183. 82 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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