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Role of TRPC6 in kidney damage after acute ischemic kidney injury

Zhihuang Zheng1,2,3, Dmitry Tsvetkov4,5,6, Theda Ulrike Patricia Bartolomaeus2,7

  • 1Department of Nephrology/Intensive Care, Charité - Universitätsmedizin Berlin, Berlin, Germany.

Scientific Reports
|February 23, 2022
PubMed

Insights

Transient Receptor Potential channel C6 (TRPC6) does not impact acute kidney injury (AKI) outcomes. TRPC6 deficiency or inhibition did not alter kidney damage markers or inflammation in mice during short-term AKI.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Transient Receptor Potential channel C6 (TRPC6) is a kidney-expressed cation channel.
  • TRPC6 gene variations are linked to chronic kidney disease.
  • The role of TRPC6 in acute kidney injury (AKI) remains unclear.

Purpose of the Study:

  • To investigate the role of TRPC6 channels in the acute phase of kidney injury.
  • To evaluate the effects of TRPC6 deficiency and pharmacological inhibition on AKI outcomes.

Main Methods:

  • Utilized Trpc6 knockout (Trpc6-/-) mice.
  • Employed pharmacological TRPC6 blockers (SH045 and BI-749327).
  • Assessed serum markers, renal epithelial damage, tubular injury, inflammation, and renal arterial myogenic tone.

Main Results:

  • Trpc6 deficiency did not affect short-term AKI outcomes.
  • Pharmacological TRPC6 inhibition showed no influence on AKI markers.
  • No significant differences were observed in renal damage, inflammation, or myogenic tone between groups.

Conclusions:

  • TRPC6 does not play a significant role in the acute phase of kidney injury.
  • TRPC6 modulation does not impact the kidney's response to acute ischemic stimuli.
  • Findings suggest potential implications for human TRPC6 gene variations in AKI context.

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