ArticleApoptosis : an international journal on programmed cell death2026
Suppression of endothelial cell PANoptosis: qingyi decoction targets the TMAO-HMGB1 pathway to mitigate lung injury in acute pancreatitis rats.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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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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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.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research status and development trends of chronic obstructive pulmonary disease and gut microbiota: a comprehensive analysis based on bibliometrics and knowledge visualization.Frontiers in microbiology · 2026Pooled it
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- From single-pathway cascade to network pathophysiology: how genetically engineered mouse models reshaped our understanding of pancreatitis.Frontiers in physiology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Trimethylamine N-oxide (TMAO) is linked to the onset and progression of acute pancreatitis (AP). Qingyi decoction (QYD) is widely used in Chinese hospitals for treating AP and its complications. This study aimed to explore the role and mechanism of QYD in alleviating severe acute pancreatitis-associated lung injury (SAP-ALI) by the modulation of the gut microbiota metabolite TMAO. The composition of the QYD was analysed using LC-MS/MS. A lung injury model in rats with SAP was created with a retrograde injection of 5% sodium taurocholate (STC, 50 mg/kg) into the pancreaticobiliary duct. The effects of exogenous TMAO, 3,3-dimethyl-l-butanol (DMB), and QYD on pulmonary microvascular endothelial barrier damage in SAP rats were assessed by ELISA, haematoxylin and eosin staining, transmission electron microscopy, RT‒qPCR, immunohistochemistry, and Western blot analysis. An in vitro model of TMAO-induced damage in HUVECs and a monocyte‒endothelial cell coculture system were created. RNA sequencing (RNA-seq) was employed to determine the impact of TMAO on the gene expression profile of endothelial cells. RT‒qPCR, Western blotting, flow cytometry, TUNEL assays, PI staining, and immunofluorescence were performed to assess whether TMAO induces endothelial cell PANoptosis and the effects of QYD on this process. The critical role of high mobility group box 1 (HMGB1) was investigated using a rescue experiment. The results demonstrated that QYD significantly alleviated pancreatic inflammation and lung injury in SAP rats, reduced TMAO levels, and effectively inhibited HMGB1-mediated pulmonary endothelial dysfunction during SAP. RNA-seq, scRNA-seq analysis and in vitro experiments confirmed that TMAO induced PANoptosis in endothelial cells. Mechanistically, QYD may exert protective effects on SAP-ALI by suppressing the TMAO-HMGB1 pathway that mediates endothelial cell PANoptosis, suggesting a potential therapeutic strategy for SAP.
Indexed as
Identifiers
41518397What 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.