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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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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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Inhibition of TRPC6 Signal Pathway Alleviates Podocyte Injury Induced by TGF-β1

Haiting Huang, Yanwu You, Xu Lin

    Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
    |February 20, 2017
    PubMed
    Abstract

    Insights

    Inhibiting transient receptor potential cation channel C6 (TRPC6) protects podocytes from transforming growth factor beta 1 (TGF-β1)-induced injury. Blocking TRPC6 reduces apoptosis and preserves nephrin expression, offering a potential therapeutic strategy for glomerulosclerosis.

    Area of Science:

    • Nephrology
    • Cell Biology
    • Molecular Biology

    Background:

    • Transforming growth factor beta 1 (TGF-β1) is implicated in glomerulosclerosis pathogenesis.
    • Podocyte injury is a key feature of glomerulosclerosis.

    Purpose of the Study:

    • To investigate the role of transient receptor potential cation channel C6 (TRPC6) in TGF-β1-induced podocyte injury.
    • To examine the effects of TRPC6 inhibition on nephrin and desmin expression in podocytes.

    Main Methods:

    • Adriamycin-induced nephropathy in rats to model glomerulosclerosis in vivo.
    • In vitro culture of podocytes treated with TGF-β1 and TRPC6 knockdown.
    • Real-time RT-PCR and Western blot to assess gene and protein expression (nephrin, desmin, caspase-9).
    • Flow cytometry and DAPI staining to evaluate podocyte apoptosis.

    Main Results:

    • TGF-β1 upregulated TGF-β1, TRPC6, desmin, and caspase-9, while decreasing nephrin in vivo and in vitro.
    • TRPC6 knockdown attenuated TGF-β1-induced increases in desmin and caspase-9 and protected nephrin.
    • TRPC6 inhibition significantly reduced podocyte apoptosis rates and morphological signs of cell death.

    Conclusions:

    • TGF-β1 induces glomerulosclerosis by altering nephrin, desmin, and caspase-9 expression via the TRPC6 pathway.
    • Inhibiting TRPC6 demonstrates a protective effect against TGF-β1-induced podocyte injury.
    • Targeting the TRPC6 signaling pathway offers a potential therapeutic avenue for glomerulosclerosis treatment.
    Keywords:
    Caspase 9DesminNephrinPodocytesTGF-β1TRPC6

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