ArticleFrontiers in immunology2021
Necroptosis Underlies Hepatic Damage in a Piglet Model of Lipopolysaccharide-Induced Sepsis.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Research trends and topics on sepsis immunosuppression: a bibliometric and visual analysis of global research from 2004 to 2024.Frontiers in medicine · 2025Pooled it
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Comparative Study of Cytokine Measurements in Blood Plasma and Serum, and Saliva of Juvenile Pigs During Experimentally Induced Acute Inflammation.Veterinary sciences · 2026Article
- Regulated cell death in sepsis-associated liver injury: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.Frontiers in immunology · 2026Review
- Neutrophil in sepsis: functional aberration and regulated cell death.Frontiers in immunology · 2026Review
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Quercetin Can Alleviate ETECK88-Induced Oxidative Stress in Weaned Piglets by Inhibiting Quorum-Sensing Signal Molecule Autoinducer-2 Production in the Cecum.Antioxidants (Basel, Switzerland) · 2025Article
- Article
- The dual role of PGAM5 in inflammation.Experimental & molecular medicine · 2025Review
- HMGB1 in Septic Muscle Atrophy: Roles and Therapeutic Potential for Muscle Atrophy and Regeneration.Journal of cachexia, sarcopenia and muscle · 2025Review
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- The dual role of neutrophils in sepsis-associated liver injury.Frontiers in immunology · 2025Review
- Mechanisms of sepsis-induced acute liver injury: a comprehensive review.Frontiers in cellular and infection microbiology · 2025Review
- Necroptosis contributes to deoxynivalenol-induced liver injury and inflammation in weaned piglets.Journal of animal science and biotechnology · 2024Article
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- From Molecular Mechanisms to Clinical Therapy: Understanding Sepsis-Induced Multiple Organ Dysfunction.International journal of molecular sciences · 2024Review
- Dysregulated dendritic cells in sepsis: functional impairment and regulated cell death.Cellular & molecular biology letters · 2024Review
- Uridine diphosphate glucuronosyltransferase 1A1 prevents the progression of liver injury.World journal of gastroenterology · 2024Article
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 at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Necroptosis is a newly recognized form of programmed cell death with characteristics of both necrosis and apoptosis. The role of necroptosis in hepatic damage during sepsis is poorly understood. In this study, we investigated the occurrence of necroptosis in hepatic damage, and its contribution to hepatic damage in a piglet model of lipopolysaccharide (LPS)-induced sepsis. Methods: Two animal experiments were conducted. In trial 1, piglets were challenged with LPS and sacrificed at different time points after LPS challenge. In trial 2, piglets were pretreated with necrostatin-1, a specific inhibitor of necroptosis, prior to LPS challenge. Alterations in the hepatic structure and function, pro-inflammatory cytokine expression, and the necroptosis signaling pathway were investigated. Typical ultrastructural characteristics of cell necrosis was observed in the liver of LPS-challenged piglets. Results: Expressions of critical components of necroptosis including kinases (RIP1, RIP3, and MLKL), mitochondrial proteins (PGAM5 and DRP1), and an intracellular damage-associated molecular pattern (HMGB1) were increased in the liver in a time-dependent manner, followed by hepatic inflammation, morphological damage, and dysfunction as manifested by elevated hepatic expression of IL-1β, IL-6 and TNF-α as well as increased serum AST and AKP activities and the AST/ALT ratio. Pretreatment with necrostatin-1 significantly reduced the expression of RIP1, RIP3 and MLKL as well as PGAM5, DRP1 and HMGB1, which subsequently led to obvious attenuation of hepatic inflammation and damage. Conclusions: Our study demonstrates that necroptosis occurs in the liver during sepsis and contributes to septic hepatic injury.
Indexed as
Identifiers
What 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.