ArticleStem cell reviews and reports2025
Mesenchymal Stem Cells Derived from Different Adipose Tissue Depots Ameliorate Severe Acute Pancreatitis by Inhibiting NF-κB/NLRP3/Caspase-1 Pathways.
Article in Stem cell reviews and reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Normal saline vs. lactated ringer's for fluid resuscitation in acute pancreatitis: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Apoptotic extracellular vesicles from peripancreatic adipose-derived mesenchymal stem cells ameliorate severe acute pancreatitis through the transcription factor EB-mediated autophagy-lysosomal pathway: an experimental study.International journal of surgery (London, England) · 2025Article
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10 authors.
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Abstract
backgroundSevere Acute Pancreatitis (SAP) is a critical gastrointestinal inflammatory disease. Mesenchymal stem cells (MSCs), multipotent cells exhibiting diverse biological properties including directional migration, paracrine signaling, immunosuppression, and anti-inflammatory effects. Adipose tissue-derived mesenchymal stem cells (ADSCs) are particularly valuable in regenerative medicine and tissue engineering. Previous studies have demonstrated that ADSCs can mitigate pancreatic damage during acute pancreatitis (AP). However, given the complexity of SAP pathophysiology, which involves a dysregulated systemic inflammatory response and multiorgan failure, the therapeutic differences and underlying mechanisms of ADSCs derived from distinct harvesting sites.
methodsThe SAP rat model was created by retrograde injection of a 4% sodium taurocholate (NaT) solution into the pancreatic duct. Rats were divided into six groups: Sham, SAP, 6 h subcutaneous ADSCs, 12 h subcutaneous ADSCs, 6 h peripancreatic ADSCs, and 12 h peripancreatic ADSCs. A total of 1 × 10
resultsADSCs from distinct harvesting site significantly attenuated inflammation in SAP rats and cell models. Compared to the SAP group, ADSCs treatment significantly lowered amylase, lipase, IL-1β, and IL-6 levels in serum and supernatants, accompanied by decrease in pancreatic histopathological scores. In vivo imaging demonstrated that peripancreatic ADSCs exhibited a 2.3-fold increase in pancreatic homing efficiency compared with subcutaneous ADSCs. Notably, 6 h peripancreatic ADSCs group showed superior therapeutic efficacy compared to other ADSCs treated rats and cell models. The therapeutic effect of ADSCs in SAP was mediated through the inhibition of NLRP3 inflammasome signaling pathways.
conclusionADSCs reduced SAP-induced pancreatic injury and inflammation by targeting NF-κB/NLRP3/Caspase-1 pathways. Early intervention with peripancreatic ADSCs demonstrated superior therapeutic efficacy, emphasizing the importance of source selection and timing of intervention.
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