ArticleInternational journal of clinical and experimental pathology2017
The renal level of a novel cytokine IL-35 is related to sepsis-associated acute kidney injury in mice.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- IL35 modulation altered survival, cytokine environment and histopathological consequences during malaria infection in mice.Malaria journal · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-35 (IL-35) is a novel immunosuppressive and anti-inflammatory cytokine. IL-35 is mainly secreted by regulatory T cells (Tregs), and exerts its effects through inducing proliferation of Tregs and reducing activity of helper T cells Th17. However, the effect of IL-35 on sepsis-associated acute kidney injury (SA-AKI) remains unclear. This study is aimed to examine the expression and role of IL-35 in an animal model of SA-AKI induced by cecal ligation and puncture (CLP). Eleven C57 male mice with SA-AKI and eight controls were used, and blood and kidney tissues were collected. Blood creatinine (Cr), urea nitrogen (BUN), alanine transaminase (ALT) and aspartate transaminase (AST) were measured to assess kidney and liver injury. The renal morphology and cell apoptosis were examined. The mRNA and protein expression levels of IL-35 in kidney tissues were tested by qRT-PCR, IHC-P, IF, and ELISA. Biochemical and histological examinations indicated CLP induced SA-AKI in mice. TUNEL assay showed apoptosis of renal tubular epithelial cells in SA-AKI mice. The mRNA and protein expression of IL-12α and EBI3 in kidney tissues decreased significantly in SA-AKI mice compared with those in sham controls. IL-35 levels in kidney tissues displayed a significantly negative correlation with the levels of Cr (
Indexed as
Identifiers
31966444PMC6965823W3013140433What OpenQuestion 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 OpenQuestion graph.