ArticleAmerican journal of translational research2022
Follistatin-like 1 ameliorates severe acute pancreatitis associated lung injury via inhibiting the activation of NLRP3 inflammasome and NF-κB pathway.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Signalling pathways regulated by FSTL1 in inflammation and potential therapeutic applications (Review).International journal of molecular medicine · 2026Review
- Article
- Nafamostat mesilate prevented caerulein-induced pancreatic injury by targeting HDAC6-mediated NLRP3 inflammasome activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Dynamic Changes in Serum Cytokine Profile in Rats with Severe Acute Pancreatitis.Medicina (Kaunas, Lithuania) · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSevere acute pancreatitis (SAP) is one of the most common abdominal conditions of digestive system that usually causes acute lung injury through systemic inflammation. Follistatin-like 1 (FSTL-1) has been reported to have anti-inflammatory and anti-apoptotic effects in a variety of diseases. The aim of this study was to investigate the effects of FSTL-1 on SAP-associated lung injury (SAPALI) and the underlying mechanism.
methodsSAP model was induced by intraperitoneal injection of the L-arginine in C57BL/6 mice. The haematoxylin and eosin (H&E) staining was applied to determine the severity of lung and pancreatic injury. ELISA kits were used to determine serum amylase and inflammatory cytokines levels. TUNEL staining was carried out to measure cell apoptosis. Western blotting was applied to analyze the related proteins of NLRP3 inflammasome and NF-κB pathways.
resultsFSTL-1 was significantly increased in the lung of SAP mice. Knockout of FSTL-1 ameliorated pancreatic injury, lung injury, inflammation and apoptosis in mice with SAP. Moreover, the protein levels of NLRP3, ASC, Caspase-1, p-p65 and p-IκBα were obviously reduced in the FSTL-1 KO+SAP group in comparison with SAP group, suggesting that inhibition of FSTL-1 repressed the activation of the NLRP3 inflammasome and NF-κB pathway.
conclusionThis study helps us understand the mechanism of FSTL-1 in SAPALI and might provide a potential new strategy for the treatment of SAPALI.
Indexed as
Identifiers
35836868PMC9274554W4285613099What OpenQuestion holds
Registered trials
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