The potential mechanism of INHBC and CSF1R in diabetic nephropathy

X-Y Du1, B-T Zheng, Y Pang

  • 1Department of Nephrology, Jining No. 1 People's Hospital, Jining, P.R. China. zhoushiju@sina.com.

Abstract

Insights

In diabetic nephropathy (DN), Inhibin beta C (INHBC) and Colony-stimulating factor 1 receptor (CSF1R) promote inflammation and inhibit apoptosis. Targeting INHBC and CSF1R may offer new therapeutic strategies for DN.

Area of Science:

  • Nephrology
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetic nephropathy (DN) is a major complication of diabetes mellitus.
  • Understanding the molecular mechanisms underlying DN is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the potential roles and mechanisms of Inhibin beta C (INHBC) and Colony-stimulating factor 1 receptor (CSF1R) in diabetic nephropathy.
  • To explore INHBC and CSF1R as potential therapeutic targets for DN.

Main Methods:

  • A diabetic nephropathy rat model was established using streptozotocin.
  • Blood glucose, insulin, biochemical markers, and inflammatory cytokines were analyzed.
  • Expression levels of INHBC, CSF1R, apoptosis-related proteins, and IGF-1 were assessed using Western blot and qPCR.

Main Results:

  • Diabetic nephropathy rats exhibited increased blood glucose, insulin, INHBC, CSF1R, IGF-1, IL-6, TNF-α, and Bcl2.
  • Levels of IL-10, Caspase 3, Caspase 9, and Bax were decreased in DN rats.
  • INHBC mRNA correlated positively with IGF-1 mRNA; CSF1R expression correlated with inflammatory and apoptotic markers.

Conclusions:

  • INHBC and CSF1R contribute to DN by inducing pro-inflammatory cytokines (IL-6, TNF-α), inhibiting anti-inflammatory cytokine (IL-10), suppressing apoptosis, and promoting renal cell proliferation.
  • INHBC and CSF1R represent promising therapeutic targets for managing diabetic nephropathy.

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