Role of TRPC6 in Progression of Diabetic Kidney Disease

Research output: Contribution to journalReview article

Details

Original languageEnglish (US)
Article number48
JournalCurrent hypertension reports
Volume21
Issue number7
StatusPublished - Jul 1 2019
Peer-reviewedYes

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.

    Research areas

  • Diabetic kidney disease, Diabetic nephropathy, Focal segmental glomerulosclerosis, TRPC6, Transient receptor potential canonical channel