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Related Experiment Video

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A High-Throughput Luciferase Assay to Evaluate Proteolysis of the Single-Turnover Protease PCSK9
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Liver fat accumulation is associated with circulating PCSK9.

Massimiliano Ruscica1, Nicola Ferri2, Chiara Macchi1

  • 1a Department of Pharmacological and Biomolecular Sciences , Università Degli Studi Di Milano , Milano , Italy ;

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Summary

Levels of circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) increase with hepatic fat accumulation in nonalcoholic fatty liver disease (NAFLD). This association is independent of metabolic factors and liver damage, suggesting PCSK9

Keywords:
LipidsNAFLDlipoproteins/metabolismlipoproteins/receptorsliver

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Area of Science:

  • Hepatology
  • Cardiovascular Disease
  • Metabolic Syndrome

Background:

  • Nonalcoholic fatty liver disease (NAFLD) is linked to cardiovascular disease, independent of traditional risk factors.
  • Proprotein convertase subtilisin/kexin type 9 (PCSK9) influences low-density lipoprotein (LDL) uptake and lipogenesis.
  • PCSK9 inhibition lowers LDL-cholesterol, highlighting its role in lipid metabolism.

Purpose of the Study:

  • To investigate the association between hepatic fat content and circulating PCSK9 levels.
  • To determine if PCSK9 levels correlate with the severity of NAFLD features.

Main Methods:

  • Analysis of 201 patients undergoing liver biopsy for suspected nonalcoholic steatohepatitis.
  • Quantification of liver damage using NAFLD activity score.
  • Measurement of circulating PCSK9 via ELISA and hepatic PCSK9 mRNA via qRT-PCR in a subset of patients.

Main Results:

  • Circulating PCSK9 levels positively correlated with steatosis grade, necroinflammation, ballooning, and fibrosis stage.
  • Multivariate analysis confirmed PCSK9 association with steatosis grade, older age, and lower BMI, independent of other factors.
  • Circulating and hepatic PCSK9 levels correlated with markers of de novo lipogenesis (SREBP-1c, FAS) and hepatic APOB.

Conclusions:

  • Circulating PCSK9 levels rise with increasing hepatic fat accumulation and correlate with steatosis severity.
  • PCSK9 may play a role in the pathogenesis of NAFLD.
  • Modulation of PCSK9 synthesis and release could be a therapeutic target in NAFLD.