Hong Wang
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Also affiliated: Hebei Medical University (2009); Army Medical University (2017); Shenzhen University (2023); Shanghai Jiao Tong University (2017); Capital Medical University (2024); Chinese Center For Disease Control and Prevention (2020); Dalian Medical University (2022); Chengde Medical University (2021); Anhui Medical University (2018); Peking University (2019); West China Medical Center of Sichuan University (2025); XinHua Hospital (2017); Beijing Jishuitan Hospital (2022); University of Alabama at Birmingham (2020); Third Affiliated Hospital of Southern Medical University (2021); West China Hospital of Sichuan University (2025); Huaian First People’s Hospital (2025); Second Hospital of Hebei Medical University (2009); Capital Institute of Pediatrics (2007); Dalian Municipal Central Hospital (2022); Jiangxi Provincial People's Hospital (2012–2024); Affiliated Hospital of Chengde Medical College (2021); Aerospace Center Hospital (2022); Hubei University of Arts and Science (2022); Beijing Anzhen Hospital (2024); Xiangyang Central Hospital (2022); Wuhan Union Hospital (2010); Peking University First Hospital (2019); First Hospital of China Medical University (2009–2011); National Institute for Viral Disease Control and Prevention (2020); Peking University Third Hospital (2016); Tongji Hospital (2014–2023); Huazhong University of Science and Technology (2007–2024); Southern Medical University (2021); Nanjing Medical University (2025); China Medical University (2011)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Hong Wang's research centers on understanding disease mechanisms and identifying biomarkers for various conditions, with a focus on cardiovascular health, bone metabolism, and infectious diseases. Wang has investigated myocardial dysfunction in COVID-19 patients using strain imaging and explored the role of ferroptosis-associated biomarkers in postmenopausal osteoporosis. Additionally, research has examined the effects of traditional Chinese medicine on COVID-19 patients and investigated genetic factors, such as RBM20 and ALPK3, associated with hypertrophic cardiomyopathy. Wang also studies the mechanisms underlying bone loss, including the impact of the WNT/β-catenin signaling pathway and filamin A, and has contributed to the development of a prognostic classification system for bone metastasis in cancer patients. Wang's work includes collaborations with Xiaolun Sun, Tahrir Alenezi, Rohana Liyanage, and Janashrit Shrestha at the University of Arkansas at Fayetteville.
Metrics
- h-index: 19
- Publications: 89
- Citations: 1,260
Selected Publications
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The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid (2025)
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Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence (2024)
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Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence (2023)
Collaboration Network
Top Collaborators
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- Potent Bile Acid Microbial Metabolites Modulate Clostridium perfringens Virulence
- Recombinant Bile Salt Hydrolase Enhances the Inhibition Efficiency of Taurodeoxycholic Acid against Clostridium perfringens Virulence
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
- The Mechanistic Target of Rapamycin Mediates Clostridium perfringens-Induced Chicken Necrotic Enteritis Attenuated by Secondary Bile Acid Deoxycholic Acid
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