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Role of TRPC6 in Progression of Diabetic Kidney Disease

  • Mechanisms of Hypertension and Target-Organ Damage (JE Hall and ME Hall, Section Editors)
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Abstract

Purpose of Review

The underlining goal of this review is to offer a concise, detailed look into current knowledge surrounding transient receptor potential canonical channel 6 (TRPC6) in the progression of diabetic kidney disease (DKD).

Recent Findings

Mutations and over-activation in TRPC6 channel activity lead to the development of glomeruli injury. Angiotensin II, reactive oxygen species, and other factors in the setting of DKD stimulate drastic increases in calcium influx through the TRPC6 channel, causing podocyte hypertrophy and foot process effacement. Loss of the podocytes further promote deterioration of the glomerular filtration barrier and play a major role in the development of both albuminuria and the renal injury in DKD. Recent genetic manipulation with TRPC6 channels in various rodent models provide additional knowledge about the role of TRPC6 in DKD and are reviewed here.

Summary

The TRPC6 channel has a pronounced role in the progression of DKD, with deviations in activity yielding detrimental outcomes. The benefits of targeting TRPC6 or its upstream or downstream signaling pathways in DKD are prominent.

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Funding

Research in the authors’ laboratories is supported by the American Heart Association 16EIA26720006, 17SDG33660149, and 18PRE34030127, the National Heart, Lung, and Blood Institute R35 HL135749, and the Department of Veteran Affairs I01 BX004024.

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Staruschenko, A., Spires, D. & Palygin, O. Role of TRPC6 in Progression of Diabetic Kidney Disease. Curr Hypertens Rep 21, 48 (2019). https://doi.org/10.1007/s11906-019-0960-9

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