ArticleScientific reports2025
The role of AIM2 inflammasome pathway-mediated pyroptosis on brain injury induced by severe acute pancreatitis in mice.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Dexmedetomidine may alleviate severe acute pancreatitis-associated lung injury by targeting the AIM2 inflammasome in endothelial cells.BMC anesthesiology · 2026Article
- Application value of blood-brain barrier and peripheral inflammatory markers in early diagnosis of pancreatic encephalopathy in severe acute pancreatitis.Frontiers in neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the role of the AIM2 inflammasome pathway-mediated pyroptosis in severe acute pancreatitis-induced brain injury (SAP-IBI) utilizing a murine model. A male C57BL/6 murine model of SAP-IBI was established. Mice were randomized into five groups: sham-operated controls (SO), SAP-IBI model, adeno-associated virus negative control (SAP + AAV-NC), AIM2 silencing via AAV-delivered shRNA (SAP + AAV-AIM2 shRNA), and AAV-mediated AIM2 overexpression (SAP + AAV-AIM2 OE). Assessment at 24 h included mortality rates, modified neurological severity scores (mNSS), histopathological scoring of pancreatic and hippocampal tissues, hippocampal water content, serum biomarkers (amylase, lipase, IL-1β, IL-18, PLA2), and expression of pyroptosis-related molecules (AIM2, ASC, Caspase-1, GSDMD, IL-1β, IL-18) in the hippocampus. At 24 h post-operation, the mortality rates of the SAP-IBI group, SAP + AAV-AIM2 shRNA group and SAP + AAV-AIM2 OE group did not reach statistical significance. Compared with the SAP-IBI group, the SAP + AAV-AIM2 shRNA group exhibited significantly improved outcomes including reduced neurological deficits (mNSS: 8.63 ± 1.06 vs. 13.00 ± 1.00; P < 0.05), markedly lower histopathological scores in both hippocampal and pancreatic tissues (P < 0.05), attenuated hippocampal edema (water content: 78.11 ± 0.45 vs. 80.70 ± 0.81; P < 0.05). These improvements were accompanied by a marked reduction in serum biomarkers (P < 0.05) and downregulation of hippocampal pyroptosis-related molecules (P < 0.05). Conversely, the SAP + AAV-AIM2 OE group showed significant exacerbation in all parameters compared to the SAP-IBI group (P < 0.05). This study demonstrates that the AIM2 inflammasome promotes hippocampal pyroptosis in SAP-IBI pathogenesis. Modulating this pathway may represent a promising therapeutic strategy for enhancing neurological outcomes.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.