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Updated: Feb 3, 2026

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells
Published on: March 7, 2025
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.
Abstract:
C1q/tumour necrosis factor-related protein-3 (CTRP3) is a member of CTRP family, and its blood level is reduced in human and rodent models of obesity and diabetes. However, the role of CTRP3 in diabetic nephropathy remains unclear. This study was designed to examine the effects of CTRP3 on cell proliferation and extracellular matrix (ECM) accumulation in human glomerular mesangial cells (MCs) in response to high glucose (HG), and explore the potential molecular mechanisms. Our results demonstrated that the expression of CTRP3 was significantly decreased by HG stimulation in MCs. In addition, CTRP3 overexpression inhibited MCs proliferation, reactive oxygen species level, and ECM production in HG-stimulated MCs. Mechanistically, CTRP3 overexpression inhibited the activation of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) pathway in HG-stimulated MCs. Taken together, these findings indicated that CTRP3 attenuated HG-induced MC proliferation and ECM production through the inactivation of the JAK2/STAT3 signaling pathway. Thus, CTRP3 may be a potential therapeutic target for the treatment of diabetic nephropathy.
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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