ArticleThe Journal of infectious diseases2017
Enhanced Glycolytic Metabolism Contributes to Cardiac Dysfunction in Polymicrobial Sepsis.
Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 156 citations in OpenAlex.
- Co-translational profiling in the cardiac endothelium in response to LPS-induced inflammation in female mice in vivo: a proof-of-concept approach.Molecular and cellular biochemistry · 2026Article
- Cytoskeletal remodeling promotes tunneling nanotube formation and drives cardiac resident cell mitochondrial transfer in sepsis.Science advances · 2026Article
- PKM2 Promotes Glycolysis in Alveolar Macrophages and Induces Inflammation in Bronchopulmonary Dysplasia.Inflammation · 2026Article
- Targeting the lactylation of ENO1 alleviates endothelial dysfunction in sepsis.Clinical and translational medicine · 2026Article
- Gut microbiota and sepsis: mechanisms, clinical correlations, and therapeutic prospects.Frontiers in medicine · 2026Article
- Lactylation modification - a bridge between sepsis and macrophage metabolic reprogramming.Frontiers in immunology · 2026Review
- Early Postnatal Stress as a Risk Factor for Cardiac Pathology in Systemic Inflammatory Conditions: An Experimental Study.Bulletin of experimental biology and medicine · 2025Article
- Integrated Transcriptome and Metabolomics Analyses Show MYC as a Potential Therapeutic Target for Behçet's Uveitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- KW-2449 Ameliorates Cardiac Dysfunction in a Rat Model of Sepsis-Induced Cardiomyopathy.Inflammation · 2025Article
- Effect of mitochondrial translocator protein TSPO on LPS-induced cardiac dysfunction.Journal of advanced research · 2025Article
- Eno1 in sepsis-induced coagulopathy: a pleiotropic mechanism hypothesis involving immunomodulation and endothelial dysfunction.Thrombosis journal · 2025Article
- Metabolism Serves as a Bridge Between Cardiomyocytes and Immune Cells in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2025Review
- H3K14la drives endothelial dysfunction in sepsis-induced ARDS by promoting SLC40A1/transferrin-mediated ferroptosis.MedComm · 2025Article
- Sepsis-induced cardiomyopathy: understanding pathophysiology and clinical implications.Archives of toxicology · 2025Review
- A murine model of acute and prolonged abdominal sepsis, supported by intensive care, reveals time-dependent metabolic alterations in the heart.Intensive care medicine experimental · 2025Article
- DANCR promotes septic cardiomyopathy by enhancing macrophage glycolytic reprogramming via the IGF2BP2/HK2 axis.Frontiers in cell and developmental biology · 2025Article
- Histone lactylation exacerbates acute lung injury in septic mice by promoting ferroptosis in pulmonary microvascular endothelial cells.Burns & trauma · 2025Article
- Decoding Sepsis: Unraveling Key Signaling Pathways for Targeted Therapies.Research (Washington, D.C.) · 2025Review
- The Protective Effect of Melatonin on LPS-Induced Myocardial InjuryCombinatorial chemistry & high throughput screening · 2025Article
- Role of pyruvate kinase M2 in regulating sepsis (Review).Molecular medicine reports · 2024Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Background: Cardiac dysfunction is present in >40% of sepsis patients and is associated with mortality rates of up to 70%. Recent evidence suggests that glycolytic metabolism plays a critical role in host defense and inflammation. Activation of Toll-like receptors on immune cells can enhance glycolytic metabolism. This study investigated whether modulation of glycolysis by inhibition of hexokinase will be beneficial to septic cardiomyopathy. Methods: Male C57B6/J mice were treated with a hexokinase inhibitor (2-deoxy-d-glucose [2-DG], 0.25-2 g/kg, n = 6-8) before cecal ligation and puncture (CLP) induced sepsis. Untreated septic mice served as control. Sham surgically operated mice treated with or without the 2-DG inhibitor served as sham controls. Cardiac function was assessed 6 hours after CLP sepsis by echocardiography. Serum was harvested for measurement of inflammatory cytokines and lactate. Results: Sepsis-induced cardiac dysfunction was significantly attenuated by administration of 2-DG. Ejection fraction and fractional shortening in 2-DG-treated septic mice were significantly (P < .05) greater than in untreated CLP mice. 2-DG administration also significantly improved survival outcome, reduced kidney and liver injury, attenuated sepsis-increased serum levels of tumor necrosis factor α and interleukin 1β as well as lactate, and enhanced the expression of Sirt1 and Sirt3 in the myocardium, which play an important role in mitochondrial function and metabolism. In addition, 2-DG administration suppresses sepsis-increased expression of apoptotic inducers Bak and Bax as well as JNK phosphorylation in the myocardium. Conclusions: Glycolytic metabolism plays an important role in mediating sepsis-induced septic cardiomyopathy. The mechanisms may involve regulation of inflammatory response and apoptotic signaling.
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.