ArticleInterdisciplinary cardiovascular and thoracic surgery2025
Mesenchymal Stromal Cells Mitigate Prolonged Cardiopulmonary Bypass-Induced Neuroinflammation.
Article in Interdisciplinary cardiovascular and thoracic surgery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Mesenchymal Stromal Cells Improve Postoperative Cardiac Dysmaturation in a Juvenile Porcine Model.Journal of the American Heart Association · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
objectivesBone marrow-derived mesenchymal stromal cell (BM-MSC) delivery through cardiopulmonary bypass (CPB) can modulate CPB-induced systemic inflammation and inhibit microglial activation. The present study assessed whether BM-MSC treatment remains effective for extensive inflammatory reactions.
methodsTwo-week-old piglets were randomized into control, CPB with deep hypothermic circulatory arrest (DHCA), CPB with BM-MSCs, CPB with DHCA plus 180 min extended perfusion, and extended CPB with BM-MSCs. Human BM-MSCs (1 × 107 cells/kg) were delivered via the CPB circuit during rewarming. We measured 9 porcine plasma cytokines. Brains were harvested for microglial immunohistochemistry and premotor cortex RNA-sequencing.
resultsA total of 20 piglets were included (n = 4 per group). An extended CPB period increased the number of white matter microglia and plasma interferon-g (IFN-g) and TNF-a levels compared to standard CPB (P < .05). Notably, BM-MSCs normalized the extensive microglia expansion resulting from prolonged CPB (P < .001). In addition to reduced IFN-g and increased IL-10, BM-MSCs increased IL-1b and IL-8 levels, suggesting possible immunosuppressive reactions observed under inflammatory microenvironment. Gene ontology analyses in the premotor cortex post-CPB found involvement of NF-kB signalling. While there was a positive correlation between IFN-g and microglia expansion/activation, IL-10 levels were inversely correlated with the number of microglia. Consistent with immunosuppressive roles in the inflammatory environment, we found inverse correlations between IL-1b and IL-8 levels and CPB-induced microglial activation (P < .01).
conclusionsBM-MSC administration via CPB shows promise for reducing extensive inflammatory stress. Further investigation using this model will elucidate CPB-induced unique pathological events in the developing brain and mechanisms underlying the therapeutic actions of BM-MSC.
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