作者: Alexander Staruschenko , Denisha Spires , Oleg Palygin
DOI: 10.1007/S11906-019-0960-9
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摘要: 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 diabetic kidney disease (DKD). Mutations and over-activation TRPC6 activity lead development glomeruli injury. Angiotensin II, reactive oxygen species, other factors setting DKD stimulate drastic increases calcium influx through channel, causing podocyte hypertrophy foot process effacement. Loss podocytes further promote deterioration glomerular filtration barrier play major role both albuminuria renal injury DKD. Recent genetic manipulation with channels various rodent models provide additional about are reviewed here. has pronounced DKD, deviations yielding detrimental outcomes. benefits targeting or its upstream downstream signaling pathways prominent.