ArticleInflammation2026
Interleukin-33 Promotes Neutrophil Extracellular Trap Formation To Aggravate Renal Ischemia-Reperfusion Injury Through ST2/PI3K/Akt and ST2/PAD4 Pathways.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Preliminary Study on the Effect of Bronchial Epithelial Cell-Released Autophagosome (BA)-Induced Neutrophils on Bronchial Epithelial Cells.Canadian respiratory journal · 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
11 authors.
Funding
Abstract
Renal ischemia-reperfusion injury (IRI) triggers a sterile immune response, primarily mediated by the innate immune system. Interleukin-33 (IL-33) promotes neutrophil infiltration during inflammatory processes, and neutrophils play a critical role in renal IRI pathology. This study aims to elucidate the mechanisms of IL-33 in neutrophil extracellular trap (NET) formation during renal IRI. The association between IL-33 and NET formation was investigated using suppression of tumorigenicity 2 (ST2) knockout (KO) mice, RNA sequencing, and pharmacological interventions. Results revealed that compared with preoperative levels, postoperative serum IL-33 and NET formation were elevated and positively correlated in patients undergoing renal transplantation. Similarly, the mouse model of renal I/R exhibited increased IL-33 expression and NET formation, which were also highly correlated. Administration of recombinant IL-33 during renal I/R enhanced NET formation and worsened renal IRI. However, treatment with an anti-IL-33 monoclonal antibody decreased NET formation and mitigated renal IRI. ST2 KO mice exhibited reduced NET formation and increased protection against renal IRI compared to control mice after renal I/R. In vitro studies showed that IL-33 dose-dependently promoted NET formation in neutrophils. Mechanistically, IL-33-induced NET formation was markedly reduced in ST2 KO mouse-derived neutrophils. Furthermore, RNA sequencing results revealed that IL-33-induced NET formation was mediated via ST2/ PI3K/Akt and ST2/peptidylarginine deiminase 4 (PAD4) signaling pathways. Inhibition of these pathways significantly suppressed IL-33-induced NET formation. In summary, this study demonstrates that IL-33/ST2 signaling exacerbates renal IRI by amplifying NETs. Targeting the IL-33/ST2 axis and inhibiting NET formation offers promising therapeutic strategies for preventing and treating renal IRI.
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.