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Metabolic Reprogramming in Toll-like Receptor-Mediated Platelet Activation.

Lih T Cheah1, Jawad S Khalil1, Mary McKay1

  • 1Discovery and Translational Science Department, Leeds Institute of Cardiovascular & Metabolic Medicine, University of Leeds, Leeds LS2 9JT, UK.

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|June 25, 2025
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Summary
This summary is machine-generated.

Platelets become highly glycolytic upon Toll-like receptor (TLR) activation, a process crucial for inflammation-driven aggregation. Targeting this metabolic shift offers a potential therapeutic strategy for TLR-initiated diseases.

Keywords:
metabolic reprogrammingplatelet activationtoll-like receptor

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Area of Science:

  • Immunology
  • Hematology
  • Metabolic pathways

Background:

  • Platelets play key roles beyond hemostasis, particularly in immunoinflammation.
  • Toll-like receptors (TLRs) on platelets initiate immune and thrombotic responses.
  • Current anti-platelet therapies risk bleeding, necessitating novel therapeutic targets.

Purpose of the Study:

  • To investigate metabolic alterations in platelets activated by Toll-like receptors (TLRs).
  • To explore the role of glycolysis and hexokinase (HK) in TLR-induced platelet activation and aggregation.

Main Methods:

  • Analysis of metabolic reprogramming in TLR1/TLR2-activated platelets.
  • Investigation of CD36-linked mechanisms in upregulated glycolysis.
  • Assessment of hexokinase (HK) role in TLR1/TLR2-induced platelet aggregation.

Main Results:

  • TLR1/TLR2 activation induces platelet glycolysis via CD36-dependent pathways.
  • Hexokinase (HK) activity is critical for TLR1/TLR2-induced platelet aggregation.
  • Platelet metabolic plasticity is altered upon TLR activation.

Conclusions:

  • TLR-induced platelet activation involves significant metabolic reprogramming towards glycolysis.
  • Targeting platelet metabolism, specifically hexokinase, may inhibit platelet function in TLR-mediated inflammatory diseases.
  • Platelet metabolic plasticity presents a novel therapeutic avenue for inflammatory conditions involving TLRs.