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Updated: Jan 20, 2026

Isolation of Human Umbilical Vein Endothelial Cells HUVEC
09:19

Isolation of Human Umbilical Vein Endothelial Cells HUVEC

Published on: April 28, 2007

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CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

Fang Wang1, Linlin Zhao1, Yingguang Shan2

  • 1Department of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Analytical Cellular Pathology (Amsterdam)
|August 21, 2019
PubMed

Insights

C1q/tumor necrosis factor-related protein 3 (CTRP3) protects against high glucose-induced endothelial dysfunction by reducing inflammation and cell death. This protection is mediated through the AKT-mTOR signaling pathway, suggesting CTRP3 as a potential therapeutic agent.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Inflammation is a key factor in diabetes-related endothelial dysfunction.
  • C1q/tumor necrosis factor-related protein 3 (CTRP3) has shown cardioprotective effects by reducing inflammation.
  • The specific role of CTRP3 in high glucose-induced endothelial dysfunction requires further investigation.

Purpose of the Study:

  • To evaluate the impact of CTRP3 on high glucose-induced inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs).
  • To elucidate the underlying molecular mechanisms, particularly the involvement of the AKT-mTOR signaling pathway.

Main Methods:

  • HUVECs were pretreated with recombinant CTRP3 and then exposed to normal or high glucose conditions.
  • Cell apoptosis, inflammatory factor production, and protein phosphorylation (AKT/mTOR) were assessed.
  • The effects of AKT inhibition and endogenous CTRP3 knockdown were also examined.

Main Results:

  • High glucose exposure reduced CTRP3 expression in HUVECs.
  • Recombinant CTRP3 treatment attenuated high glucose-induced inflammation and apoptosis.
  • CTRP3 enhanced AKT/mTOR phosphorylation, and this effect was blocked by AKT inhibition.
  • Knockdown of CTRP3 exacerbated high glucose-induced inflammation and reduced cell viability.

Conclusions:

  • CTRP3 treatment mitigates high glucose-induced endothelial inflammation and apoptosis via the AKT-mTOR signaling pathway.
  • CTRP3 demonstrates potential as a therapeutic agent for preventing diabetes-related endothelial dysfunction.
Abstract

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