scholarly journals Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Qian Wang ◽  
Xuefei Tian ◽  
Yuyang Wang ◽  
Yan Wang ◽  
Jialin Li ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Actin Cytoskeleton ◽  
Diabetic Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Diabetic Kidney ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor ◽  
Cytoskeleton Rearrangement

Podocyte injury is an important pathogenesis step causing proteinuric kidney diseases such as diabetic kidney disease (DKD). Actin cytoskeleton rearrangement in podocyte induced by multiple pathogenic factors is believed to be the key process resulting in glomerular injury. Many studies have recently shown that transient receptor potential canonical channel 6 (TRPC6) in podocyte plays a critical role in the development and progression of proteinuric kidney disease by regulating its actin cytoskeleton rearrangement. This review is aimed at summarizing the role of TRPC6 on DKD by regulating the podocyte actin cytoskeleton rearrangement, thereby help further broaden our views and understanding on the mechanism of DKD and provide a theoretic basis for exploring new therapeutic targets for DKD patients.

scholarly journals Examining the role of transient receptor potential canonical 5 (TRPC5) in osteoarthritis

2020 ◽  
Vol 2 (4) ◽  
pp. 100119
Author(s):  
João de Sousa Valente ◽  
Khadija M. Alawi ◽  
Patrik Keringer ◽  
Sabah Bharde ◽  
Faseeha Ayaz ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor

The role of transient receptor potential channels in kidney disease

2009 ◽  
Vol 5 (8) ◽  
pp. 441-449 ◽  
Author(s):  
Titia E. Woudenberg-Vrenken ◽  
René J. M. Bindels ◽  
Joost G. J. Hoenderop
Keyword(s):  
Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Potential Channels ◽  
Transient Receptor

scholarly journals Protective role of Trpc6 knockout in the progression of diabetic kidney disease

2018 ◽  
Vol 315 (4) ◽  
pp. F1091-F1097 ◽  
Author(s):  
Denisha Spires ◽  
Daria V. Ilatovskaya ◽  
Vladislav Levchenko ◽  
Paula E. North ◽  
Aron M. Geurts ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Protective Role ◽  
Glomerular Injury ◽  
Diabetic Kidney ◽  
Channel Inhibition ◽  
Trpc6 Channel ◽  
Stage Renal Disease

Diabetic kidney disease (DKD) is a chronic kidney pathology that leads to end-stage renal disease. Previous studies from our laboratory indicate that there is an association between the development of DKD and the transient receptor potential canonical 6 (TRPC6) channel. Trpc6 expression and activity were increased in the streptozotocin (STZ)-treated Dahl Salt-sensitive (Dahl SS) rat, an established model of type 1 diabetes. Here, using a Trpc6 knockout created on the Dahl SS rat background (SSTrpc6−/−), we test the hypothesis that the absence of Trpc6 will protect podocytes and kidney function during the development of DKD. Four groups of animals (control SSWT, SSTrpc6−/−, STZ-treated SSWT, and STZ-SSTrpc6−/−) were utilized in this study. Diabetes development was monitored for 11 wk after STZ injection with periodic weight, glucose, and urinary output measurements. There was an increase in albuminuria and glomerular injury following STZ treatment, which was not different between Dahl SS and SSTrpc6−/− groups. Western blot analysis revealed elevated levels of nephrin in urine samples of STZ-SSWT rats, which was higher compared with STZ-SSTrpc6−/− rats. Furthermore, pathological increases in basal [Ca2+]i levels and foot process damage of podocytes during the development of DKD was attenuated in the STZ-SSTrpc6−/− compared with STZ-SSWT rats. Overall, our data indicate that TRPC6 channel inhibition may have at least partial renoprotective effects, which could lead to the development of new pharmacological tools to treat or prevent the progression of DKD.

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