Abstract
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). 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. 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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