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Updated: Feb 20, 2026

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli
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TRPC5 Does Not Cause or Aggravate Glomerular Disease.

Xuexiang Wang1, Ranadheer R Dande1, Hao Yu1

  • 1Department of Medicine, Rush University Medical Center, Chicago, Illinois.

Journal of the American Society of Nephrology : JASN
|October 25, 2017
PubMed
Summary
This summary is machine-generated.

Overexpressing or activating the TRPC5 ion channel did not harm kidney function in mice. These findings suggest TRPC5 does not cause kidney barrier injury, even under disease conditions.

Keywords:
TRPC5calcium channelsglomerular diseaseglomerular filtration barrierpodocyteproteinuria

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Transient receptor potential channel 5 (TRPC5) is involved in calcium influx and cell migration, with notable expression in the brain and kidney.
  • TRPC5 dysfunction benefits kidney filter dynamics by modulating podocyte cytoskeletal remodeling.
  • Limited in vivo gain-of-function studies exist regarding TRPC5's role in kidney function.

Purpose of the Study:

  • To investigate the in vivo effects of TRPC5 gain-of-function on kidney function and integrity.
  • To determine if TRPC5 overexpression or activation exacerbates kidney barrier injury.

Main Methods:

  • Development of two transgenic mouse models overexpressing wild-type or a TRPC5 ion-pore mutant.
  • Assessment of proteinuria and LPS-induced albuminuria at 8 months of age.
  • Evaluation of TRPC5 activation (Englerin A) and inhibition (ML204) effects on kidney injury markers.

Main Results:

  • Transgenic mice overexpressing TRPC5 showed no increased proteinuria at 8 months compared to controls.
  • Neither TRPC5 overexpression nor activation with Englerin A led to increased proteinuria.
  • Inhibition of TRPC5 with ML204 did not significantly alter LPS-induced albuminuria.

Conclusions:

  • TRPC5 overexpression or activation does not induce kidney barrier injury in mice.
  • TRPC5 modulation does not aggravate kidney injury under pathological conditions like LPS challenge.
  • These findings clarify the role of TRPC5 in kidney physiology and pathology.