ArticleInflammation2023
Pyruvate Dehydrogenase Kinase 2 Accelerates Endotoxin Shock by Promoting Mitogen-Activated Protein Kinase Activation.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 11 citations in OpenAlex.
- The Dual Role of Natural Killer Cells in the Septic Liver.Journal of inflammation research · 2026Review
- Identifying potential drug targets for sepsis-related adult respiratory distress syndrome through comprehensive genetic analysis and druggability assessment.Journal of global health · 2025Article
- Atractylenolide I prevents acute liver failure in mouse by regulating M1 macrophage polarization.Scientific reports · 2025Article
- Multi-omics derivation of a core gene signature for predicting therapeutic response and characterizing immune dysregulation in inflammatory bowel disease.Frontiers in immunology · 2025Article
- Article
- The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury.Frontiers in immunology · 2024Review
- An overview of the mechanisms and potential roles of extracellular vesicles in septic shock.Frontiers in immunology · 2023Review
- Pyruvate dehydrogenase kinase regulates macrophage polarization in metabolic and inflammatory diseases.Frontiers in immunology · 2023Review
- Activation of Kupffer cells in NAFLD and NASH: mechanisms and therapeutic interventions.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxin shock remains one of the major causes of mortality worldwide. Pyruvate dehydrogenase kinase (PDK) 2 is an important regulatory enzyme involved in glucose metabolism. The purpose of this study was to determine the regulatory effect of PDK2 on LPS-induced endotoxin shock and explore the mechanisms in vivo and in vitro. Here, we showed that PDK2 contributed to Toll-like receptor (TLR)-mediated inflammation. Lipopolysaccharide (LPS) activation of TLR4 pathways resulted in PDK2 upregulation in macrophages and dendritic cells (DCs). PDK2 overexpression enhanced TLR4 signaling pathway activation, whereas downregulating PDK2 expression inhibited TLR4 signaling pathway activation. Pharmacological inhibition of PDK2 significantly decreased the mortality rate and alleviated pathological injury in the lungs and livers of LPS-challenged mice, while significantly suppressing proinflammatory cytokine production. Thus, we confirmed that PDK2 is involved in LPS-induced endotoxin shock by modulating TLR4-mitogen-activated protein kinase signaling and inducing the production of proinflammatory cytokines in macrophages and DCs. Our findings highlight the importance of PDK2 as a novel target to treat septic shock.
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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.