Neural Regeneration Research ›› 2026, Vol. 21 ›› Issue (7): 2820-2821.doi: 10.4103/NRR.NRR-D-25-00442

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Valosin-containing protein, neural proteopathies, and implications for neural regeneration

Jae-Geun Lee, Eun-Ji Lee, Hoon Ryu, Jeong-Soo Lee*   

  1. Microbiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea (Lee JG, Lee EJ, Lee JS) KRIBB School, University of Science and Technology, Daejeon, Republic of Korea (Lee EJ, Lee JS) Center for Brain Disorders, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea (Ryu H) KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul, Republic of Korea (Ryu H)
  • Online:2026-07-15 Published:2025-10-20
  • Contact: Jeong-Soo Lee, PhD, jeongsoo@kribb.re.kr.
  • Supported by:
    The authors thank our current lab members for thoughtful discussion on the manuscript. This work was supported by a grant of the Korea Dementia Research Project through the Korea Dementia Research Center (RS-2022-KH126506 to JSL), the ABC-based Regenerative BioTherapeutics (ABC project) grant (RS-2024-00426031 to JSL), and NRF Grant (2022R1A2C3013138 to HR, RS2024-00449723 to JGL) funded by the Korea government (the Ministry of Health & Welfare, Ministry of Science and ICT, and Ministry of Education).

Abstract: Proteostasis, also known as protein homeostasis, is a tightly regulated cellular quality control process that ensures the balance of protein synthesis, folding, posttranslational modifications, and degradation. Maintaining proteostasis is vital for cellular function, organismal health, and longevity. The disruption of proteostasis can lead to a range of detrimental effects, including accelerated aging, compromised cellular function, and even cell death, manifesting in numerous human diseases (Hipp et al., 2019). Neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases (AD, PD, HD, respectively), are often characterized by the accumulation of misfolded proteins that aggregate into granules or inclusions. These aggregates form when proteins lose their proper conformation and fail to be refolded or degraded efficiently due to the failure of proteostasis. The persistence of these pathological protein aggregates can interfere with cellular processes, disrupt organelle function, and ultimately contribute to disease progression (Hipp et al., 2019).