ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Forsythoside E Alleviates Liver Injury by Targeting PKM2 Tetramerization to Promote Macrophage M2 Polarization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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.
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Who cites it
4 citing papers in PubMed.
- Uhrf1-Mediated PKM2 Degradation via Ubiquitination Alleviates Inflammation and Pyroptosis in Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Interaction networks of macrophage glycolysis and inflammation in sepsis: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Forsythoside E Alleviates Liver Injury by Targeting PKM2 Tetramerization to Promote Macrophage M2 Polarization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The spatiotemporal dynamic evolution of post-stroke neuroinflammation: energy metabolism mechanisms of acute response and chronic progression.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Sepsis-induced liver injury is closely associated with poor prognosis in septic patients. In this study, through integrated approaches including high-throughput virtual screening, target fishing technology, and atomic force microscopy (AFM) analysis, Forsythiaside E (FE) is first identified as a novel allosteric activator of pyruvate kinase M2 (PKM2) that promotes tetramer formation. Mutant protein construction combined with dynamic light scattering (DLS) and fluorescence resonance energy transfer (FRET) reveals FE binds to PKM2 K311 to promote tetramer formation. Employing Seahorse XF metabolic analyzers, real-time single-cell multi-modal analysis systems, and transcriptome sequencing, it is revealed that FE-mediated PKM2 tetramerization induces metabolic reprogramming in macrophages while suppressing STAT3 phosphorylation and subsequent NLRP3 transcriptional activation. In vivo assessments indicate that FE exhibited no significant multi-organ toxicity. FE alleviates sepsis-induced liver injury by promoting macrophage polarization toward the M2 anti-inflammatory phenotype. Further validation through macrophage-specific overexpression of PKM2 WT/K311A in mice confirms FE's mechanism of action. Collectively, this study elucidates the molecular mechanism by which FE alleviates sepsis-associated liver injury through targeted PKM2 tetramerization and proposes an innovative metabolic-epigenetic coordinated regulation strategy for sepsis-related liver injury treatment.
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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 Socratic graph.