Chao-Chao Yu

Chao-Chao Yu

*This is an algorithmically generated author record based on publicly available information.

Current Organizations / Institutes

The organizations/institutes from the scholar's latest article

Previous Organizations / Institutes

The organizations / institutes from the scholar's other articles in the past ten years


Chao-Chao Yu has a total of 74 co-authors. Here are the top co-authors by number of shared publications:

  • Li-Hong Kong

    College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China

    9 shared publications
  • Jia Wang

    Department of Acupuncture and Moxibustion, Wuhan Hospital of Integrated Traditional Chinese and Western Medicine, Wuhan, China

    5 shared publications
  • Rui Han

    Department of Child Rehabilitation Medicine, Qujing Hospital of Maternity and Childcare, Qujing, China

    5 shared publications
  • Yan-Jun Du

    College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China

    5 shared publications
  • Feng Shen

    College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, 430061, China

    4 shared publications
  • Aofei Yang

    Department of Orthopedics, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei, 430061, China; Department of Orthopedics, Affiliated Hospital of Hubei University of Chinese Medicine, Wuhan, Hubei, 430061, China

    3 shared publications

Latest Publications

  • Open Access

    Erratum to: Electroacupuncture Alleviates Memory Deficits in APP/PS1 Mice by Targeting Serotonergic Neurons in Dorsal Raphe Nucleus

    by Chao‑Chao Yu, Xiao‑Fei Wang, Jia Wang, Chu Li, Juan Xiao, Xue‑Song Wang, Rui Han, Shu‑Qin Wang, Yuan‑Fang Lin, Li‑Hong Kong, et al.

  • Open Access

    Corrigendum: Neural circuit mechanisms of acupuncture effect: where are we now?

    by Xuesong Wang, Jia Wang, Rui Han, Chaochao Yu, Feng Shen, \Nxuesong Wang

    Corrigendum: Neural circuit mechanisms of acupuncture effect: where are we now?* Correspondence: Chaochao Yu kiterunner2@163.com; Feng Shen 40052958@qq.comKeywords: same as original article Corrigendum on: Wang X, Wang J, Han R, Yu C and Shen F (2024) Neural circuit mechanisms of acupuncture effect: where are we now? Front. Neurol. 15:1399925. doi: 10.3389/fneur.2024.1399925 Incorrect Funding In the published article, there was an error in the Funding statement. [This work was funded by Shenzhen Science and Technology Program (No. 2021- 22154) ;National Natural Science Foundation of China (No. 82205271); Key Chinese Medicine Project supported by Hubei Provincial Natural Science Foundation (2023AFD113); Chinese Medicine Research Project supported by Hubei Administration of Traditional Chinese Medicine, China (No. ZY2023F138).]. The correct Funding statement appears below.FUNDING[This work was funded by Shenzhen Science and Technology Program (No. JCYJ20210324111609024) ;National Natural Science Foundation of China (No. 82205271); Key Chinese Medicine Project supported by Hubei Provincial Natural Science Foundation (2023AFD113); Chinese Medicine Research Project supported by Hubei Administration of Traditional Chinese Medicine, China (No. ZY2023F138).]The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.


  • Open Access

    Erratum to: Electroacupuncture Alleviates Memory Deficits in APP/PS1 Mice by Targeting Serotonergic Neurons in Dorsal Raphe Nucleus

    by Chao-Chao Yu, Xiao-Fei Wang, Jia Wang, Chu Li, Juan Xiao, Xue-Song Wang, Rui Han, Shu-Qin Wang, Yuan-Fang Lin, Li-Hong Kong, et al.

  • Electroacupuncture Alleviates Memory Deficits in APP/PS1 Mice by Targeting Serotonergic Neurons in Dorsal Raphe Nucleus

    by Chao-Chao Yu, Xiao-Fei Wang, Jia Wang, Chu Li, Juan Xiao, Xue-Song Wang, Rui Han, Shu-Qin Wang, Yuan-Fang Lin, Li-Hong Kong, et al.

    Objective Alzheimer’s disease (AD) has become a significant global concern, but effective drugs able to slow down AD progression is still lacked. Electroacupuncture (EA) has been demonstrated to ameliorate cognitive impairment in individuals with AD. However, the underlying mechanisms remains poorly understood. This study aimed at examining the neuroprotective properties of EA and its potential mechanism of action against AD. Methods APP/PS1 transgenic mice were employed to evaluate the protective effects of EA on Shenshu (BL 23) and Baihui (GV 20). Chemogenetic manipulation was used to activate or inhibit serotonergic neurons within the dorsal raphe nucleus (DRN). Learning and memory abilities were assessed by the novel object recognition and Morris water maze tests. Golgi staining, western blot, and immunostaining were utilized to determine EA-induced neuroprotection. Results EA at Shenshu (BL 23) and Baihui (GV 20) effectively ameliorated learning and memory impairments in APP/PS1 mice. EA attenuated dendritic spine loss, increased the expression levels of PSD95, synaptophysin, and brain-derived neurotrophic factor in hippocampus. Activation of serotonergic neurons within the DRN can ameliorate cognitive deficits in AD by activating glutamatergic neurons mediated by 5-HT1B. Chemogenetic inhibition of serotonergic neurons in the DRN reversed the effects of EA on synaptic plasticity and memory. Conclusion EA can alleviate cognitive dysfunction in APP/PS1 mice by activating serotonergic neurons in the DRN. Further study is necessary to better understand how the serotonergic neurons-related neural circuits involves in EA-induced memory improvement in AD.


  • Open Access

    Neural circuit mechanisms of acupuncture effect: where are we now?

    by Xuesong Wang, Jia Wang, Rui Han, Chaochao Yu, Feng Shen

    Recently, there has been increasing attention on the impact of acupuncture on the dysregulated neural circuits in different disease. This has led to new understandings of how acupuncture works. This review presents a comprehensive analysis of research that have examined the impact of acupuncture on abnormal neural circuits associated with pain, anxiety, Parkinson’s disease, addiction disorders, cognitive problems, and gastrointestinal disorders. These studies have shown that acupuncture’s therapeutic effects are mediated by specific brain areas and neurons involved in neural circuit mechanisms, emphasising its wide-ranging influence. The positive impacts of acupuncture can be ascribed to its ability to modify the functioning of neurocircuits in various physiological conditions. Nevertheless, contemporary studies on acupuncture neural circuits frequently overlook the comprehensive circuit mechanism including the periphery, central nervous system, and target organ. Additionally, the scope of diseases studied is restricted. Future study should focus on broadening the range of diseases studied and exploring the neural circuit mechanisms of these diseases in depth in order to enhance our understanding of acupuncture’s neurobiological impacts.


  • Bioactive constituents of animal-derived traditional Chinese medicinal materials for breast cancer: opportunities and challenges

    by Chaochao Yu, Yi Li, Guopeng Chen, Chaoyan Wu, Xiuping Wang, Yingwen Zhang

    Breast cancer is globally the most common invasive cancer in women and remains one of the leading causes of cancer-related deaths. Surgery, radiotherapy, c


  • Open Access

    Investigation of Anti-Epithelial-Mesenchymal Transition and Anti-Inflammation effects of Qing Fei Hua Xian Decotion on Pulmonary Fibrosis via Network Pharmacology and Experimental Verification

    by Chao-Chao Yu, Rui-Jie Li, Xiao-Fei Wang, Chao-Yan Wu, Yan-Fang Peng, Xiu-Ping Wang, Wei Chen, Lian-Guo Ruan, Ying-Wen Zhang

    Background Pulmonary fibrosis (PF) is a common interstitial pneumonia disease, also occurred in post-COVID-19 survivors. The mechanism underlying the anti-PF effect of Qing Fei Hua Xian Decotion (QFHXD), a traditional Chinese medicine formula applied for treating PF in COVID-19 survivors, is unclear. This study aimed to uncover the mechanisms related to the anti-PF effect of QFHXD through analysis of network pharmacology and experimental verification. Methods The candidate chemical compounds of QFHXD and its putative targets for treating PF were achieved from public databases, thereby we established the corresponding “herb- compound -target” network of QFHXD. Moreover, The protein–protein interaction (PPI) network of potential targets was also constructed to screen the core targets. Furthermore, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were used to predict targets, and pathways, then validated by in vivo experiments. Results A total of 188 active compounds in QFHXD and 50 target genes were identified from databases. The key therapeutic targets of QFHXD, such as PI3K/Akt, IL-6, TNF, IL-1β, STAT3, MMP-9, and TGF-β1 were identified by KEGG and GO analysis. Anti-PF effects of QFHXD (in a dose-dependent manner) and prednisone were confirmed by HE, Masson staining, and Sirius red staining as well as in vivo Micro-CT and immunohistochemical analysis in a rat model of bleomycin-induced PF. Besides, QFXHD remarkably inhibits the activity of PI3K/Akt/NF-κB and TGF‑β1/Smad2/3. Conclusion QFXHD significantly attenuated bleomycin-induced PF via inhibiting inflammation and EMT. PI3K/Akt/NF-κB and TGF‑β1/Smad2/3 pathways might be the potential therapeutic effects of QFHXD for treating PF.

  • Open Access

    Epigenetic Modulation of Microglia Function and Phenotypes in Neurodegenerative Diseases

    by Li Wang, Chao-Chao Yu, Xin-Yuan Liu, Xiao-Ni Deng, Qing Tian, Yan-Jun Du

    Microglia-mediated neuroinflammation is one of the most remarkable hallmarks of neurodegenerative diseases (NDDs), including AD, PD, and ALS. Accumulating evidence indicates that microglia play both neuroprotective and detrimental roles in the onset and progression of NDDs. Yet, the specific mechanisms of action surrounding microglia are not clear. Modulation of microglia function and phenotypes appears to be a potential strategy to reverse NDDs. Until recently, research into the epigenetic mechanisms of diseases has been gradually developed, making it possible to elucidate the molecular mechanisms underlying the epigenetic regulation of microglia in NDDs. This review highlights the function and phenotypes of microglia, elucidates the relationship between microglia, epigenetic modifications, and NDDs, as well as the possible mechanisms underlying the epigenetic modulation of microglia in NDDs with a focus on potential intervention strategies.


  • Open Access

    Genome‐Wide Regulation of Electroacupuncture and Treadmill Exercise on Diet‐Induced Obese Rats

    by Yanji Zhang, Jia Li, Dan Wei, Guoyan Mo, Chaochao Yu, Lihua Wang, Yue Zhuo, Kou Xu, Yingrong Zhang, Yixuan Xue, et al.

    Acupuncture has been widely used for obesity treatment, but its mechanism is still unclear. To investigate the molecular mechanisms, we applied electroacupuncture (EA) at the Zusanli (ST36) acupoint and treadmill exercise (TE) in a diet‐induced obese (DIO) rat model and used RNA sequencing (RNA‐seq) to identify molecular consequences. Forty Sprague‐Dawley male rats were selected and randomly divided into five groups: control (C), DIO model (M), EA, TE, and EA + TE groups. According to the results, acupuncture reduced body weight and the ratio of retroperitoneal white adipose tissue (retro‐WAT) to body weight. Total RNA was extracted from the retro‐WAT from five groups for RNA‐seq. Differentially expressed genes (DEG) analysis showed that there were obvious differences among the four comparisons of C vs. M, M vs. EA, M vs. TE, and M vs. EA + TE, followed by 1383, 913, 3324, and 2794 DE genes. Gene ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed to further classify the DEGs. Several GO terms were commonly significantly enriched in both M vs. TE and M vs. EA, such as myofibril and muscle contraction. In addition, some pathways were regulated by EA and TE, such as the peroxisome proliferator activated receptor signaling pathway and calcium signaling pathway. This study is the first to compare and analyze the differences in gene expression profiles in the retro‐WAT of rats in different groups, which provide a clue for further investigation into the molecular mechanisms of obesity treatment by EA and TE.


  • Open Access

    Preventive Electroacupuncture Ameliorates D‐Galactose‐Induced Alzheimer’s Disease‐Like Pathology and Memory Deficits Probably via Inhibition of GSK3β/mTOR Signaling Pathway

    by Chao-Chao Yu, Jia Wang, Si-Si Ye, Shan Gao, Jia Li, Li Wang, Tao Jiang, Xue-Song Wang, Bo-Cun Li, Qing Shu, et al.

    Acupuncture has been practiced to treat neuropsychiatric disorders for a thousand years in China. Prevention of disease by acupuncture and moxibustion treatment, guided by the theory of Chinese acupuncture, gradually draws growing attention nowadays and has been investigated in the role of the prevention and treatment of mental disorders such as AD. Despite its well‐documented efficacy, its biological action remains greatly invalidated. Here, we sought to observe whether preventive electroacupuncture during the aging process could alleviate learning and memory deficits in D‐galactose‐induced aged rats. We found that preventive electroacupuncture at GV20‐BL23 acupoints during aging attenuated the hippocampal loss of dendritic spines, ameliorated neuronal microtubule injuries, and increased the expressions of postsynaptic PSD95 and presynaptic SYN, two important synapse‐associated proteins involved in synaptic plasticity. Furthermore, we observed an inhibition of GSK3β/mTOR pathway activity accompanied by a decrease in tau phosphorylation level and prompted autophagy activity induced by preventive electroacupuncture. Our results suggested that preventive electroacupuncture can prevent and alleviate memory deficits and ameliorate synapse and neuronal microtubule damage in aging rats, which was probably via the inhibition of GSK3β/mTOR signaling pathway. It may provide new insights for the identification of prevention strategies of AD.