The role and mechanisms of mesenchymal stem cells in postoperative cognitive dysfunction via immune network regulation
Postoperative cognitive dysfunction (POCD) is a common neurological complication in elderly patients after surgery. Its pathophysiology is complex. Neuroinflammation, oxidative stress, and immune imbalance are all involved in this process. These changes can affect postoperative recovery and reduce patients’ quality of life. As population aging continues to increase, the prevention and treatment of POCD have become important clinical issues. In recent years, mesenchymal stem cells (MSCs) have attracted attention in neurological diseases because of their immunomodulatory and tissue healing abilities. Current studies suggest that MSCs may relieve neuroinflammation, protect neurons, and improve cognitive function by regulating the immune network. This regulation includes modulating T cell function, promoting macrophage polarization toward an anti-inflammatory phenotype, and maintaining cytokine balance. However, the mechanisms by which MSCs act in POCD have not been fully clarified. Their clinical application also faces several challenges, including transplantation efficiency, long-term safety, and individualized treatment design. Therefore, this review summarizes how MSCs may intervene in POCD through immune network regulation. This review also aims to provide a theoretical basis and possible research directions for future studies in this field.
Authors
- Chengran Wang (ORCID: https://orcid.org/0009-0003-2120-9452)
- Fanglei Han
- Lizheng Huang (ORCID: https://orcid.org/0009-0009-2409-4885)
- Shanshan Yu
- Xuehao Liu
- Jinlan Jiang
- Haiqi Song
Institutions
- Union Hospital (HK)
- Shanghai First Maternity and Infant Hospital (CN)
- Union Hospital (CN)
Publication Details
- Journal
- Stem Cell Research & Therapy
- Published
- 2026-09-10
- DOI
- https://doi.org/10.1186/s13287-026-05294-w
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00