ArticleShock (Augusta, Ga.)2014
Early murine polymicrobial sepsis predominantly causes renal injury.
Article in Shock (Augusta, Ga.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
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
27 citing papers in PubMed, 40 citations in OpenAlex.
- A neonatal mouse model of meconium peritonitis generated using human meconium slurry.Pediatric research · 2025Article
- INHIBITING SIRT2 ATTENUATES SEPSIS-INDUCED ACUTE KIDNEY INJURY VIA FOXO1 ACETYLATION-MEDIATED AUTOPHAGY ACTIVATION.Shock (Augusta, Ga.) · 2025Article
- Herpes virus entry mediator signaling blockade produces mortality in neonatal sepsis through induced cardiac dysfunction.Frontiers in immunology · 2024Article
- Shock drives a STAT3 and JunB-mediated coordinated transcriptional and DNA methylation response in the endothelium.Journal of cell science · 2023Article
- The Novel Compound SUL-138 Counteracts Endothelial Cell and Kidney Dysfunction in Sepsis by Preserving Mitochondrial Function.International journal of molecular sciences · 2023Article
- Lymphocyte HVEM/BTLA co-expression after critical illness demonstrates severity indiscriminate upregulation, impacting critical illness-induced immunosuppression.Frontiers in medicine · 2023Article
- A two-hit model of sepsis plus hyperoxia causes lung permeability and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Endothelial SOCS3 maintains homeostasis and promotes survival in endotoxemic mice.JCI insight · 2021Article
- Sepsis Biomarkers.Methods in molecular biology (Clifton, N.J.) · 2021Review
- Apoptotic cell therapy for cytokine storm associated with acute severe sepsis.Cell death & disease · 2020Article
- The role of activated NLRP3 inflammatory body in acute kidney injury in rats caused by sepsis and NLRP3-TXNIP signaling pathway.Saudi journal of biological sciences · 2020Article
- Protein kinase C-delta inhibition is organ-protective, enhances pathogen clearance, and improves survival in sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.International journal of molecular sciences · 2019Review
- Effects of salbutamol and phlorizin on acute pulmonary inflammation and disease severity in experimental sepsis.PloS one · 2019Article
- Delayed activation of PPAR-β/δ improves long-term survival in mouse sepsis: effects on organ inflammation and coagulation.Innate immunity · 2018Article
- The role of adenosine 1a receptor signaling on GFR early after the induction of sepsis.American journal of physiology. Renal physiology · 2018Article
- Sepsis-3 on the Block: What Does It Mean for Preclinical Sepsis Modeling?Shock (Augusta, Ga.) · 2017Article
- Current Murine Models of Sepsis.Surgical infections · 2016Review
- Nonhematopoietic Peroxisome Proliferator-Activated Receptor-α Protects Against Cardiac Injury and Enhances Survival in Experimental Polymicrobial Sepsis.Critical care medicine · 2016Article
- Innate Immune Molecule Surfactant Protein D Attenuates Sepsis-induced Acute Pancreatic Injury through Modulating Apoptosis and NF-κB-mediated Inflammation.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Multiple organ failure in sepsis substantially increases mortality. This study examined if there was greater hepatic, pancreatic, splenic, or renal injury in mice that would die during sepsis induced by cecal ligation and puncture (CLP) compared with that of those that would survive. Mice were stratified into groups predicted to die (Die-P) or predicted to live (Live-P) in the first 5 days after CLP based on plasma interleukin 6 levels. Groups were sacrificed to harvest organs for histology. Separate animals were followed for survival with daily blood sampling to examine renal function. No significant histological evidence of organ injury was observed in either the Live-P or Die-P mice. Minimal hepatic injury occurred as plasma aspartate transaminase demonstrated less than a 2-fold increase over normal in both groups. In addition, pancreatic injury was minimal as there was also less than a 2-fold increase in plasma amylase levels. In contrast, blood urea nitrogen levels were nearly five times higher within 24 h in Die-P mice compared with those of mice predicted to live. Mice with blood urea nitrogen levels higher than 44 mg/dL had a 17.6 higher relative risk of dying (95% confidence interval, 4.5-69.4). Cystatin C, a more specific kidney function biomarker, was also elevated at 24 h after CLP. When the cystatin C levels were analyzed relative to the hours before death, rather than hours after CLP, they were also significantly increased in mice Dead by day 5 compared with those Alive after day 5. We conclude that limited liver, pancreas, and spleen injury develops during murine CLP-induced sepsis while significant kidney injury is present. The renal injury becomes worse closer to death.
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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.