Related Experiment Video

Updated: Jul 14, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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CTRP4 attenuates apoptosis and epithelial-mesenchymal transition markers in podocytes through an

Wonjun Cho1, Heeseung Oh1, Sung Woo Choi1

  • 1Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, Republic of Korea.

Biochemical and Biophysical Research Communications
|October 8, 2023
PubMed

Insights

C1q/TNF-related protein 4 (CTRP4) reduces high glucose-induced podocyte apoptosis and endoplasmic reticulum (ER) stress. This protective effect in diabetic nephropathy is mediated by activating the AMPK/autophagy pathway.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Endocrinology

Background:

  • Hyperglycemia is a key factor in diabetic nephropathy development, causing podocyte damage.
  • Endoplasmic reticulum (ER) stress and apoptosis in podocytes contribute to kidney disease progression.
  • C1q/TNF-related protein 4 (CTRP4) exhibits anti-obesity and anti-inflammatory effects.

Purpose of the Study:

  • To investigate CTRP4's effects on podocyte apoptosis and ER stress under high glucose conditions.
  • To elucidate the underlying molecular mechanisms, including AMPK and autophagy signaling.

Main Methods:

  • Western blotting to assess protein expression in podocytes and adipocytes.
  • MDC staining for autophagosome detection and Hoechst staining for chromatin condensation.
  • Cellular experiments involving CTRP4 treatment, AMPK silencing, and autophagy inhibition (3-MA).

Main Results:

  • High glucose increased CTRP4 expression in adipocytes and podocytes.
  • CTRP4 treatment reduced high glucose-induced podocyte apoptosis, ER stress, and normalized EMT markers.
  • CTRP4 elevated AMPK phosphorylation and autophagy; blocking these pathways diminished CTRP4's protective effects.

Conclusions:

  • CTRP4 alleviates hyperglycemic ER stress and podocyte apoptosis.
  • The protective mechanism involves the AMPK/autophagy signaling pathway.
  • CTRP4 shows therapeutic potential for managing diabetic nephropathy.
Keywords:
AMPKApoptosisAutophagyCTRP4NephropathyPodocyte

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