ArticleInternational journal of clinical and experimental pathology2019
Protective role of JNK inhibitor SP600125 in sepsis-induced acute lung injury.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 20 citations in OpenAlex.
- Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.Histology and histopathology · 2025Article
- Fused in Sarcoma (FUS) promotes renal cell carcinoma progression via the KCMF1/FUS/CENPT axis and activation of the JNK signaling pathway.Journal of translational medicine · 2025Article
- C5a Induces Inflammatory Signaling and Apoptosis in PC12 Cells through C5aR-Dependent Signaling: A Potential Mechanism for Adrenal Damage in Sepsis.International journal of molecular sciences · 2024Article
- Protective effects of nordalbergin against LPS-induced endotoxemia through inhibiting MAPK/NF-κB signaling pathway, NLRP3 inflammasome activation, and ROS production.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Silencing circPalm2 inhibits sepsis-induced acute lung injury by sponging miR-376b-3p and targeting MAP3K1.Toxicological research · 2023Article
- Acute respiratory distress syndrome heterogeneity and the septic ARDS subgroup.Frontiers in immunology · 2023Review
- Extracellular histone H3 facilitates ferroptosis in sepsis through ROS/JNK pathway.Immunity, inflammation and disease · 2023Article
- Exosomes Derived from ADSCs Attenuate Sepsis-Induced Lung Injury by Delivery of Circ-Fryl and Regulation of the miR-490-3p/SIRT3 Pathway.Inflammation · 2022Article
- Classic Signaling Pathways in Alveolar Injury and Repair Involved in Sepsis-Induced ALI/ARDS: New Research Progress and Prospect.Disease markers · 2022Review
- Downregulation of miR-223 promotes HMGB2 expression and induces oxidative stress to activate JNK and promote autophagy in an in vitro model of acute lung injury.Journal of inflammation (London, England) · 2021Article
- Apoptosis signal-regulating kinase 1 (ASK1) inhibition reduces endothelial cytokine production without improving permeability after toll-like receptor 4 (TLR4) challenge.Translational research : the journal of laboratory and clinical medicine · 2021Article
- Article
- Expression of DUSP12 Reduces Lung Vascular Endothelial Cell Damage in a Murine Model of Lipopolysaccharide-Induced Acute Lung Injury via the Apoptosis Signal-Regulating Kinase 1 (ASK1)-Jun N-Terminal Kinase Activation (JNK) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy.The Lancet. Respiratory medicine · 2020Review
- MiR-140 Resensitizes Cisplatin-Resistant NSCLC Cells to Cisplatin Treatment Through the SIRT1/ROS/JNK Pathway.OncoTargets and therapy · 2020Article
- C-Jun N-terminal kinase inhibitors: Structural insight into kinase-inhibitor complexes.Computational and structural biotechnology journal · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhether the c-Jun N-terminal kinase (JNK) pathway mediates apoptosis in sepsis-induced acute lung injury is not known. Here we investigated the effect of JNK inhibition in a rat model of sepsis-induced lung injury, and assessed expression of JNK and endoplasmic reticulum stress-related proteins.
methodsSepsis was established by cecal ligation and puncture (CLP) in 48 male Sprague-Dawley rats. 32 additional rats underwent sham surgery. 24 CLP rats and 24 sham rats received tail vein injection of 30 mg/kg SP600125. The rest received saline injection. At 6, 12 and 24 h after surgery, blood, bronchoalveolar lavage fluid (BALF) and lung tissue were collected. p-JNK, XBP-1, ATF-4 and CHOP levels of the lung tissue were measured by western blot; and the JNK mRNA levels were measured by qPCR.
resultsThe W/D ratios of lungs in the CLP group were significantly higher than those in the sham group, but lower those in the CLP+JNK inhibitor group (P<0.05). TUNEL staining revealed significantly more apoptotic cells in the lungs of the CLP group than the sham group, and in the CLP+JNK inhibitor group the apoptotic index was significantly reduced (P<0.05). XBP-1, ATF-4, CHOP and p-JNK protein levels and JNK mRNA levels were significantly elevated in the CLP group (P<0.05), but significantly ameliorated in the CLP+JNK inhibitor group (P<0.05).
conclusionsInhibition of the JNK signaling pathway mitigates sepsis-induced lung injury. Our results suggest that JNK signaling promotes endoplasmic reticulum stress and thus apoptosis in sepsis-induced lung injury.
Indexed as
Identifiers
31933857PMC6945091W3008977274What 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.