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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

Updated: Jun 26, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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TRPC6 Knockout Alleviates Renal Fibrosis through PI3K/AKT/GSK3B Pathway.

An-Bang Sun1,2, Fang-Hua Li3, Lin Zhu1,2

  • 1Department of Anatomy, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Current Medical Science
|May 15, 2024
PubMed
Summary
This summary is machine-generated.

Ablating transient receptor potential channel 6 (TRPC6) reduces kidney fibrosis by decreasing tubular epithelial cell apoptosis and inflammation. This occurs via the down-regulation of the PI3K/AKT/GSK3β pathway, suggesting TRPC6 as a therapeutic target for chronic kidney disease.

Keywords:
ischemia-reperfusion injuryrenal fibrosisrenal tubular epithelial cellstransient receptor potential channel 6

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Renal fibrosis is a common endpoint for various kidney injuries.
  • Transient receptor potential channel 6 (TRPC6) has shown potential in mitigating renal fibrosis, but its regulatory role is not fully understood.

Purpose of the Study:

  • To investigate the impact of TRPC6 knockout on renal fibrosis.
  • To elucidate the underlying mechanisms by which TRPC6 influences renal fibrosis progression.

Main Methods:

  • Utilized unilateral renal ischemia-reperfusion (uIR) injury in TRPC6 knockout (TRPC6-/-) and wild-type (WT) mice.
  • Assessed primary tubular epithelial cells (PTECs) from TRPC6-/- and WT mice treated with transforming growth factor β1 (TGFβ1).
  • Evaluated fibrotic markers, apoptosis, inflammation, and the PI3K/AKT/GSK3β signaling pathway using histological and molecular techniques.

Main Results:

  • TRPC6 expression was elevated in uIR mice and TGFβ1-treated PTECs.
  • TRPC6-/- significantly alleviated renal fibrosis, reducing fibrotic markers (Col-1, α-SMA, vimentin), apoptosis, and inflammation in PTECs.
  • The PI3K/AKT/GSK3β signaling pathway was down-regulated in TRPC6-ablated models.

Conclusions:

  • TRPC6 ablation mitigates renal fibrosis by inhibiting PTEC apoptosis and inflammation.
  • Down-regulation of the PI3K/AKT/GSK3β pathway is a key mechanism in TRPC6's anti-fibrotic effect.
  • Targeting TRPC6 presents a potential therapeutic strategy for chronic kidney disease prevention.