ArticleMediators of inflammation2020
Reevaluation of Lung Injury in TNF-Induced Shock: The Role of the Acid Sphingomyelinase.
Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Sodium thiosulfate does not affect energy metabolism or organ (dys)function during resuscitation from murine trauma-and-hemorrhage.Intensive care medicine experimental · 2025Article
- Mouse Model of Nitrogen Mustard Ocular Surface Injury Characterization and Sphingolipid Signaling.International journal of molecular sciences · 2024Article
- The role of sphingolipids in meibomian gland dysfunction and ocular surface inflammation.The ocular surface · 2022Review
- Article
- Reference Gene Selection for Gene Expression Analyses in Mouse Models of Acute Lung Injury.International journal of molecular sciences · 2021Article
- Tumor necrosis factor-α requires Ezrin to regulate the cytoskeleton and cause pulmonary microvascular endothelial barrier damage.Microvascular research · 2021Article
- The Impact of Dietary Sphingolipids on Intestinal Microbiota and Gastrointestinal Immune Homeostasis.Frontiers in immunology · 2021Review
- Keep Your Friends Close, but Your Enemies Closer: Role of Acid Sphingomyelinase During Infection and Host Response.Frontiers in medicine · 2020Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor (TNF) is a well-known mediator of sepsis. In many cases, sepsis results in multiple organ injury including the lung with acute respiratory distress syndrome (ARDS). More than 20-year-old studies have suggested that TNF may be directly responsible for organ injury during sepsis. However, these old studies are inconclusive, because they relied on human rather than conspecific TNF, which was contaminated with endotoxin in most studies. In this study, we characterized the direct effects of intravenous murine endotoxin-free TNF on cardiovascular functions and organ injury in mice with a particular focus on the lungs. Because of the relevance of the acid sphingomyelinase in sepsis, ARDS, and caspase-independent cell death, we also included acid sphingomyelinase-deficient (ASM
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Registered trials
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