ArticleCell2017
Metabolic Adaptation Establishes Disease Tolerance to Sepsis.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 2 of them syntheses that pooled it.
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
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
180 citing papers in PubMed, 2 syntheses or guidelines pooled it, 272 citations in OpenAlex.
- The efficacy and safety of qiwei baizhu san in the treatment of type 2 diabetes mellitus: a systematic review and meta-analysis.Frontiers in pharmacology · 2024Pooled it
- Update in Hyperferritinemic Syndromes: Recognition and Management - A Scoping Review.The Brown journal of hospital medicine · 2022Pooled it
- ARISE framework: a temporal, multi-organ view of perfusion in sepsis.Internal and emergency medicine · 2026Review
- Ferroptosis is a Physiologic Vulnerability of Iron-Recycling Macrophages.bioRxiv : the preprint server for biology · 2026Article
- Article
- Hypomorphic biliverdin reductase a mutations define bilirubin anti-malarial threshold.iScience · 2026Article
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Measuring signatures of host resistance, disease tolerance, and damage in human sepsis: a prospective cohort study.Intensive care medicine · 2026Article
- Differential disease tolerance mediates sex-biased illness severity in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Negative Correlation Between Serum Ferritin and CD4+ Lymphocytes: A Retrospective Study on Kikuchi-Fujimoto Disease.Immunity, inflammation and disease · 2026Article
- Article
- A Nomogram Prediction Model and Validation of Hypoglycemia Risk in Patients With Decompensated Cirrhosis and Type 2 Diabetes.Journal of diabetes research · 2026Article
- Article
- The mechanisms by which free heme exacerbates sepsis and the potential therapeutic targets.Frontiers in immunology · 2026Review
- The immunology of sepsis: translating new insights into clinical practice.Nature reviews. Nephrology · 2026Review
- Mitochondria-immunometabolism in sepsis-induced liver injury: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Multi-omics analysis identifies PPARα as a key inhibitor of hepatocyte ferroptosis in sepsis-associated liver injury.PloS one · 2026Article
- Understanding metabolic resilience by unraveling temporal dynamics of cellular responses.Trends in endocrinology and metabolism: TEM · 2025Review
- Lipoxin A4 alleviates sepsis-induced acute liver injury by inhibiting inflammatory response and iron overload via JAK2/STAT3 signaling.Scientific reports · 2025Article
120 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Sepsis is an often lethal syndrome resulting from maladaptive immune and metabolic responses to infection, compromising host homeostasis. Disease tolerance is a defense strategy against infection that preserves host homeostasis without exerting a direct negative impact on pathogens. Here, we demonstrate that induction of the iron-sequestering ferritin H chain (FTH) in response to polymicrobial infections is critical to establish disease tolerance to sepsis. The protective effect of FTH is exerted via a mechanism that counters iron-driven oxidative inhibition of the liver glucose-6-phosphatase (G6Pase), and in doing so, sustains endogenous glucose production via liver gluconeogenesis. This is required to prevent the development of hypoglycemia that otherwise compromises disease tolerance to sepsis. FTH overexpression or ferritin administration establish disease tolerance therapeutically. In conclusion, disease tolerance to sepsis relies on a crosstalk between adaptive responses controlling iron and glucose metabolism, required to maintain blood glucose within a physiologic range compatible with host survival.
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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.