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TRPM7 contributes to progressive nephropathy.

Sayuri Suzuki1,2, Reinhold Penner3,4,5, Andrea Fleig3,4,5

  • 1Center for Biomedical Research, The Queen's Medical Center, 1301 Punchbowl St., Honolulu, HI, 96813, USA. sayuris@hawaii.edu.

Scientific Reports
|February 13, 2020
PubMed
Summary
This summary is machine-generated.

Transient Receptor Potential Melastatin 7 (TRPM7) channel kinase is upregulated in kidney fibrosis. Inhibiting TRPM7 with NS8593 protects against kidney damage and fibrosis by reducing cell proliferation and inflammation.

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Area of Science:

  • Physiology
  • Molecular Biology
  • Pathology

Background:

  • Transient Receptor Potential Melastatin 7 (TRPM7) is an ion channel with kinase activity.
  • TRPM7 is implicated in various diseases and overexpressed in fibrotic conditions.
  • Its specific role in kidney fibrosis remains largely unknown.

Purpose of the Study:

  • To investigate the role of TRPM7 in kidney fibrosis using a unilateral ureteral obstruction (UUO) mouse model.
  • To determine if TRPM7 inhibition can ameliorate renal damage and fibrosis.

Main Methods:

  • Utilized the UUO mouse model to induce kidney injury and fibrosis.
  • Administered NS8593, a TRPM7 inhibitor, systemically.
  • Assessed kidney morphology, tubular formation, cell proliferation, and TGF-β1/Smad signaling.

Main Results:

  • TRPM7 expression was significantly increased in UUO kidneys.
  • NS8593 treatment prevented kidney atrophy and preserved tubular structures in UUO kidneys.
  • TRPM7 inhibition reduced tubular and interstitial cell proliferation and suppressed TGF-β1/Smad signaling.

Conclusions:

  • TRPM7 is upregulated during inflammatory renal damage and contributes to kidney fibrosis.
  • Pharmacological targeting of TRPM7 offers a potential therapeutic strategy for progressive kidney fibrosis.