Related Experiment Video

Updated: Jun 15, 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

368

ALKBH5-Mediated m6A Modification Drives Apoptosis in Renal Tubular Epithelial Cells by Negatively Regulating MUC1

Wenwei Chen1,2,3, Changyi Liu1,2,3, Yanfeng He1,2,3

  • 1Department of Urology, Urology Research Institute, The First Affiliated Hospital, Fujian Medical University, Chazhong Road 20, Taijiang District, Fuzhou, 350005, Fujian, People's Republic of China.

Molecular Biotechnology
|August 22, 2024
PubMed

Insights

Overexpression of ALKBH5 promotes renal tubular epithelial cell apoptosis by reducing m6A modification, impacting Mucin 1 (MUC1) stability and the PI3K/Akt pathway. This reveals a new therapeutic target for kidney stones.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Nephrology

Background:

  • Renal tubular epithelial cell (RTEC) apoptosis is crucial in nephrolithiasis pathogenesis.
  • N6-methyladenosine (m6A) modification's role in RTEC injury and apoptosis is under-investigated.

Purpose of the Study:

  • To investigate the role of ALKBH5 in RTEC apoptosis.
  • To elucidate the molecular mechanisms underlying ALKBH5-mediated RTEC apoptosis.

Main Methods:

  • Overexpression of ALKBH5 in RTEC cells.
  • Measurement of m6A modification levels.
  • Analysis of Mucin 1 (MUC1) mRNA stability and expression.
  • Investigation of the PI3K/Akt signaling pathway.

Main Results:

  • ALKBH5 overexpression reduced m6A levels in RTEC cells, promoting apoptosis.
  • ALKBH5 decreased m6A modification on MUC1 mRNA, impairing its stability and expression.
  • The ALKBH5-MUC1 axis promoted RTEC apoptosis via the PI3K/Akt pathway.

Conclusions:

  • The ALKBH5-MUC1-PI3K/Akt regulatory system plays a critical role in RTEC apoptosis.
  • This pathway presents potential therapeutic targets for nephrolithiasis treatment.
Keywords:
ALKBH5ApoptosisMUC1N6-methyladenosineNephrolithiasisPI3K/Akt

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