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Related Experiment Video

Updated: Sep 7, 2025

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CPT2 K79 acetylation regulates platelet life span.

Xuemei Fan1, Yang Wang1, Xiaohong Cai2

  • 1Department of Biochemistry and Molecular Cell Biology, and.

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Platelet storage lesion is caused by long-chain acylcarnitines (LCACs) accumulation, which damages mitochondria. Targeting LCAC generation improves platelet storage and extends posttransfusion survival.

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Area of Science:

  • Biochemistry
  • Hematology
  • Cellular Biology

Background:

  • Platelet transfusion services face challenges due to the short lifespan of platelets.
  • Mitochondrial damage and platelet storage lesion contribute to reduced platelet viability.

Purpose of the Study:

  • To investigate the role of long-chain acylcarnitines (LCACs) in platelet storage lesion.
  • To identify mechanisms underlying LCAC accumulation and mitochondrial damage in platelets.
  • To explore therapeutic strategies for improving platelet storage quality.

Main Methods:

  • Investigated the link between fatty acid oxidation, AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase/carnitine palmitoyltransferase 1 (CPT1) pathways, and LCAC accumulation.
  • Elucidated the role of NAD+ exhaustion, sirtuin 3 (Sirt3) activity, and CPT2 acetylation in blocking fatty acid oxidation.
  • Tested inhibitors of AMPK or CPT1, Sirt3 agonists, and antioxidants in vitro and in vivo models.

Main Results:

  • Accumulation of LCACs was identified as a key factor in mitochondrial damage and platelet storage lesion.
  • Blockade of fatty acid oxidation, driven by AMPK/CPT1 pathway activation, leads to LCAC accumulation.
  • CPT2 K79 acetylation, resulting from NAD+ depletion and decreased Sirt3 activity, inhibits fatty acid oxidation and promotes LCAC buildup.
  • Interventions targeting LCAC generation significantly reduced platelet storage lesion and improved posttransfusion survival.

Conclusions:

  • CPT2 acetylation impairs fatty acid oxidation, worsening platelet storage lesion.
  • Targeting CPT2 acetylation presents a novel therapeutic strategy for enhancing platelet storage quality and extending platelet lifespan.