Neuroinflammation is a key factor in the development of preterm white matter injury (PWMI), leading to glial cell dysfunction, arrest of oligodendrocyte maturation, and long-term neurological damage. As a potential therapeutic strategy, mesenchymal stem cells (MSCs) exhibit significant immunomodulatory and regenerative potential. Recent studies suggest that the primary mechanism of MSC action is their paracrine effects, particularly mediated by extracellular vesicles, with MSC-derived exosomes (MSC-Exos) being the key mediators. MSC-Exos, enriched with lipids, proteins, and nucleic acids, regulate neuroinflammation by modulating glial cell activity and influencing signaling pathways associated with inflammation and repair. Preclinical evidence has indicated that MSC-Exos can suppress the activation of microglia and astrocytes, promote oligodendrocyte maturation, and enhance myelination, highlighting their potential as a cell-free treatment for PWMI. However, there are a paucity of comprehensive reviews on how MSC-Exos regulate neuroinflammation in PWMI through specific signaling pathways. This review aims to summarize the key signaling pathways through which MSC-Exos modulate neuroinflammation in PWMI and discuss the challenges associated with the clinical application of MSC-Exos-based therapies.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10571-025-01540-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The transcription factor GmbZIP131 enhances soybean salt tolerance by regulating flavonoid biosynthesis.
Plant Physiol
March 2025
College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Detoxifying reactive oxygen species (ROS) that accumulate under saline conditions is crucial for plant salt tolerance. The Salt Overly Sensitive (SOS) pathway functions upstream, while flavonoids act downstream, in ROS scavenging under salt stress. However, the potential crosstalk between the SOS pathway and flavonoids in regulating salt stress responses and the associated mechanisms remain largely unexplored.
View Article and Find Full Text PDFThe ERN1 signaling pathway of unfolded protein controls the expression of EDEM1 and its hypoxic regulation in glioblastoma cells.
Endocr Regul
January 2025
1Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
For the effective growth of malignant tumors, including glioblastoma, the necessary factors involve endoplasmic reticulum (ER) stress, hypoxia, and the availability of nutrients, particularly glucose. The ER degradation enhancing alpha-mannosidase like protein 1 (EDEM1) is involved in ER-associated degradation (ERAD) targeting misfolded glycoproteins for degradation in an N-glycan-independent manner. EDEM1 was also identified as a new modulator of insulin synthesis and secretion.
View Article and Find Full Text PDFEffects of PARP1 inhibitor PJ-34 on TGFα, IL-6, and IL-1β levels in diabetic nephropathy.
J Immunol
February 2025
Orthopedics Department, Central Hospital of Ezhou, Ezhou, China.
Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β.
View Article and Find Full Text PDFInnateness transcriptome gradients characterize mouse T lymphocyte populations.
J Immunol
February 2025
La Jolla Institute for Immunology, La Jolla, CA, United States.
A fundamental dichotomy in lymphocytes separates adaptive T and B lymphocytes, with clonally expressed antigen receptors, from innate lymphocytes, which carry out more rapid responses. Some T cell populations, however, are intermediates between these 2 poles, with the capacity to respond rapidly through T cell receptor activation or by cytokine stimulation. Here, using publicly available datasets, we constructed linear mixed models that not only define a gradient of innate gene expression in common for mouse innate-like T cells, but also are applicable to other mouse T lymphoid populations.
View Article and Find Full Text PDFCo-Exposure to Polystyrene Microplastics and Bisphenol A Contributes to the Formation of Liver Fibrosis in Mice through Inhibition of the BMAL1/E-Cad Signaling Pathway.
J Agric Food Chem
March 2025
Northwest A&F University, Yangling, Shaanxi 712100, China.
The food safety risks posed by exposure to polystyrene microplastics (PS-MPs) and bisphenol A (BPA) have become an issue worldwide. However, the toxic effects of PS-MPs and BPA coexposure on the mammalian liver remain elusive. In this study, we found that PS-MPs and BPA coexposure have synergistic toxic effects on AML12 cells and the mouse liver.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!