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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

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Role of TRPC6 in Progression of Diabetic Kidney Disease

Alexander Staruschenko1,2, Denisha Spires3, Oleg Palygin3

  • 1Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226, USA. staruschenko@mcw.edu.

Current Hypertension Reports
|May 23, 2019
PubMed
Abstract

Insights

Transient Receptor Potential Canonical channel 6 (TRPC6) exacerbates diabetic kidney disease (DKD) by increasing calcium influx, leading to podocyte injury and kidney damage. Targeting TRPC6 offers potential therapeutic benefits for DKD progression.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Diabetic kidney disease (DKD) is a major complication of diabetes, characterized by progressive kidney damage.
  • Podocyte injury and dysfunction are central to DKD pathogenesis, leading to albuminuria and renal failure.

Purpose of the Study:

  • To review current knowledge on the role of Transient Receptor Potential Canonical channel 6 (TRPC6) in DKD progression.
  • To elucidate the mechanisms by which TRPC6 contributes to glomerular injury in DKD.

Main Methods:

  • Review of existing literature on TRPC6 function in DKD.
  • Analysis of genetic manipulation studies in rodent models of DKD.

Main Results:

  • TRPC6 over-activation and mutations contribute to glomeruli injury in DKD.
  • Increased calcium influx via TRPC6 causes podocyte hypertrophy and foot process effacement.
  • TRPC6 plays a significant role in albuminuria and renal injury development in DKD.

Conclusions:

  • TRPC6 has a pronounced role in DKD progression, with dysregulated activity leading to detrimental outcomes.
  • Targeting TRPC6 or its signaling pathways presents a promising therapeutic strategy for managing DKD.
Keywords:
Diabetic kidney diseaseDiabetic nephropathyFocal segmental glomerulosclerosisTRPC6Transient receptor potential canonical channel

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