CTRP3 inhibits high glucose-induced human glomerular mesangial cell dysfunction

Tian-Ying Hu1, La-Mei Li2, Yan-Zi Pan3

  • 1Department of Endocrinology, Weinan Central Hospital, Weinan, Shaanxi, China.

Insights

C1q/tumour necrosis factor-related protein-3 (CTRP3) levels decrease in diabetes. CTRP3 protects against high glucose-induced kidney cell damage by inhibiting proliferation and extracellular matrix buildup via the JAK2/STAT3 pathway.

Area of Science:

  • Endocrinology
  • Nephrology
  • Molecular Biology

Background:

  • C1q/tumour necrosis factor-related protein-3 (CTRP3) levels are reduced in obesity and diabetes.
  • The role of CTRP3 in diabetic nephropathy is not well understood.

Purpose of the Study:

  • To investigate the effect of CTRP3 on human glomerular mesangial cells (MCs) under high glucose conditions.
  • To explore the molecular mechanisms underlying CTRP3's action in diabetic nephropathy.

Main Methods:

  • Assessed CTRP3 expression in MCs stimulated with high glucose.
  • Overexpressed CTRP3 in MCs to evaluate its impact on proliferation, reactive oxygen species (ROS), and extracellular matrix (ECM) production.
  • Investigated the involvement of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) pathway.

Main Results:

  • High glucose significantly decreased CTRP3 expression in MCs.
  • CTRP3 overexpression inhibited MC proliferation, ROS levels, and ECM accumulation in high glucose-treated MCs.
  • CTRP3 overexpression suppressed the activation of the JAK2/STAT3 signaling pathway.

Conclusions:

  • CTRP3 attenuates high glucose-induced MC proliferation and ECM production.
  • CTRP3 exerts its protective effects by inactivating the JAK2/STAT3 signaling pathway.
  • CTRP3 represents a potential therapeutic target for diabetic nephropathy.

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