Wu Hong-Wei, Chen He-Dan, Chen Ya-Hong, Mao Xin-Li, Feng Yu-Yi, Li Shao-Wei, Zhou Xian-Bin
Department of Infectious Diseases, Taizhou Enze Medical Center (Group) Enze Hospital, Taizhou, Zhejiang, China.
Department of Infectious Diseases, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, Zhejiang, China.
Stem Cells Int. 2023 May 11;2023:4586398. doi: 10.1155/2023/4586398. eCollection 2023.
Mesenchymal stem cells have shown noticeable potential for unlimited self-renewal. They can differentiate into specific somatic cells, integrate into target tissues via cell-cell contact, paracrine effects, exosomes, and other processes and then regulate the target cells and tissues. Studies have demonstrated that transplantation of MSCs could decrease the expression and concentration of collagen in the liver, thereby reducing liver fibrosis. A growing body of evidence indicates that apoptotic MSCs could inhibit harmful immune responses and reduce inflammatory responses more effectively than viable MSCs. Accumulating evidence suggests that mitochondrial transfer from MSCs is a novel strategy for the regeneration of various damaged cells via the rescue of their respiratory activities. This study is aimed at reviewing the functions of MSCs and the related roles of the programmed cell death of MSCs, including autophagy, apoptosis, pyroptosis, and ferroptosis, as well as the regulatory pathogenic mechanisms of MSCs in liver fibrosis. Research has demonstrated that the miR-200B-3p gene is differentially expressed gene between LF and normal liver samples, and that the miR-200B-3p gene expression is positively correlated with the degree of liver fibrosis, suggesting that MSCs could inhibit liver fibrosis through pyroptosis. It was confirmed that circulating monocytes could deliver MSC-derived immunomodulatory molecules to different sites by phagocytosis of apoptotic MSCs, thereby achieving systemic immunosuppression. Accordingly, it was suggested that characterization of the programmed cell death-mediated immunomodulatory signaling pathways in MSCs should be a focus of research.
间充质干细胞已显示出无限自我更新的显著潜力。它们可以分化为特定的体细胞，通过细胞间接触、旁分泌作用、外泌体等过程整合到靶组织中，进而调节靶细胞和组织。研究表明，间充质干细胞移植可降低肝脏中胶原蛋白的表达和浓度，从而减轻肝纤维化。越来越多的证据表明，凋亡的间充质干细胞比活的间充质干细胞能更有效地抑制有害免疫反应并减轻炎症反应。越来越多的证据表明，间充质干细胞的线粒体转移是通过挽救各种受损细胞的呼吸活动来实现其再生的一种新策略。本研究旨在综述间充质干细胞的功能以及间充质干细胞程序性细胞死亡的相关作用，包括自噬、凋亡、焦亡和铁死亡，以及间充质干细胞在肝纤维化中的调节致病机制。研究表明，miR-200B-3p基因是肝纤维化样本与正常肝脏样本之间的差异表达基因，且miR-200B-3p基因表达与肝纤维化程度呈正相关，提示间充质干细胞可通过焦亡抑制肝纤维化。已证实循环单核细胞可通过吞噬凋亡的间充质干细胞将间充质干细胞衍生的免疫调节分子传递至不同部位，从而实现全身免疫抑制。因此，间充质干细胞中程序性细胞死亡介导的免疫调节信号通路的特征应成为研究的重点。
