Current Organizations / Institutes

The organizations/institutes from the scholar's latest article


Yiheng Wang has a total of 6 co-authors. Here are the top co-authors by number of shared publications:

  • Hanyu Li

    Hunan Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China

    1 shared publication
  • Mei Yang

    Hunan Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China

    1 shared publication
  • Wei Hu

    Department of Integrated Traditional Chinese and Western Medicine, Xiangya Boai Rehabilitation Hospital, Changsha 410151, China

    1 shared publication
  • Xiaoxu Yang

    Hunan Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China

    1 shared publication
  • Xihua Cheng

    Hunan Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China

    1 shared publication
  • Yancheng Zhong

    Hunan Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China

    1 shared publication

Latest Publications

  • Open Access

    The Interaction Between Insulin Resistance and Neuroinflammation in the Brain and Its Impact on Diabetic Encephalopathy

    by Yiheng Wang, Hanyu Li, Xiaoxu Yang, Mei Yang, Wei Hu, Xihua Cheng, Yancheng Zhong

    Diabetic encephalopathy (DE) is a severe complication of diabetes mellitus affecting the central nervous system (CNS), characterized by cognitive dysfunction. This review systematically explores how the interplay between brain insulin resistance (BIR) and neuroinflammation contributes to the pathogenesis of DE. BIR refers to the diminished responsiveness of the CNS to insulin signaling, resulting in the suppression of the PI3K/Akt and MAPK pathways, impaired glucose metabolism, and dysfunction across multiple neural cell types—including neurons, astrocytes, microglia, brain endothelial cells, and oligodendrocytes. These disturbances manifest as impaired energy metabolism, compromised synaptic plasticity, disruption of the blood–brain barrier, and reduced myelination. Importantly, BIR and neuroinflammation form a vicious cycle within these cells, mutually exacerbating each other and jointly driving the pathological progression of DE. Finally, we have compiled a list of currently available drugs that can improve BIR and suppress neuroinflammation, along with the latest progress in clinical trials, to provide new insights for the future of precision treatment for DE.