scholarly journals Multiprotein Complex With TRPC (Transient Receptor Potential-Canonical) Channel, PDE1C (Phosphodiesterase 1C), and A2R (Adenosine A2 Receptor) Plays a Critical Role in Regulating Cardiomyocyte cAMP and Survival

Circulation ◽  
2018 ◽  
Vol 138 (18) ◽  
pp. 1988-2002 ◽  
Author(s):  
Yishuai Zhang ◽  
Walter Knight ◽  
Si Chen ◽  
Amy Mohan ◽  
Chen Yan
Keyword(s):  
Transient Receptor Potential ◽  
Critical Role ◽  
Receptor Potential ◽  
Multiprotein Complex ◽  
Transient Receptor Potential Canonical ◽  
Adenosine A2 Receptor ◽  
Transient Receptor

scholarly journals TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases

2015 ◽  
Vol 309 (5) ◽  
pp. F393-F397 ◽  
Author(s):  
Daria V. Ilatovskaya ◽  
Alexander Staruschenko
Keyword(s):  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Kidney Diseases ◽  
Critical Role ◽  
Receptor Potential ◽  
Calcium Flux ◽  
Calcium Handling ◽  
Podocyte Injury ◽  
Trpc6 Channel ◽  
Transient Receptor

Podocytes (terminally differentiated epithelial cells of the glomeruli) play a key role in the maintenance of glomerular structure and permeability and in the incipiency of various renal abnormalities. Injury to podocytes is considered a major contributor to the development of kidney disease as their loss causes proteinuria and progressive glomerulosclerosis. The physiological function of podocytes is critically dependent on proper intracellular calcium handling; excessive calcium influx in these cells may result in the effacement of foot processes, apoptosis, and subsequent glomeruli damage. One of the key proteins responsible for calcium flux in the podocytes is transient receptor potential cation channel, subfamily C, member 6 (TRPC6); a gain-of-function mutation in TRPC6 has been associated with the onset of the familial forms of focal segmental glomerulosclerosis (FSGS). Recent data also revealed a critical role of this channel in the onset of diabetic nephropathy. Therefore, major efforts of the research community have been recently dedicated to unraveling the TRPC6-dependent effects in the initiation of podocyte injury. This mini-review focuses on the TRPC6 channel in podocytes and colligates recent data in an attempt to shed some light on the mechanisms underlying the pathogenesis of TRPC6-mediated glomeruli damage and its potential role as a therapeutic target for the treatment of chronic kidney diseases.

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