Yingying Wang
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Also affiliated: Anhui University (2011–2021); University of Shanghai for Science and Technology (2019); Chinese Academy of Medical Sciences & Peking Union Medical College (2017); Nankai University (2013); Fudan University (2019); Beijing Normal University (2014–2017); Naval Aeronautical and Astronautical University (2020); Jining Medical University (2022); Southeast University (2008); University of Hong Kong (2004); China National Petroleum Corporation (China) (2023)
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Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Yingying Wang's research focuses on developing novel senolytic compounds, agents designed to selectively eliminate senescent cells, which are implicated in various age-related diseases. Her work has involved the design and optimization of piperlongumine analogs as potent senolytics. Additionally, Wang has investigated the in vitro activity of Vernonia cumingiana Benth. Her publications also extend to materials science, including work on enhancing the thermal and mechanical properties of polymethyl methacrylate (PMMA)/graphene nanoplatelets (GNPs) nanocomposites for electronic component radiators, and improving the thermally conductive and microwave absorbing properties of PMMA/Ni@GNP nanocomposites. Wang holds a h-index of 8 with 24 publications and 753 citations.
Metrics
- h-index: 8
- Publications: 24
- Citations: 784
Selected Publications
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Design and optimization of piperlongumine analogs as potent senolytics (2023)
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Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice (2017)
Collaboration Network
Top Collaborators
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Design and optimization of piperlongumine analogs as potent senolytics
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice
- Design and optimization of piperlongumine analogs as potent senolytics
- Design and optimization of piperlongumine analogs as potent senolytics
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