TRPC6 – a new podocyte gene involved in focal segmental glomerulosclerosis
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TRPC6
Glomerulosclerosis
Glomerulosclerosis
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TRPC6
Klotho
Ectopic expression
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Recent studies have shown that transient receptor potential cation channel 6(TRPC6) expressed in podocytes,and located in slit diaphragm,it colocalized with nephrin,podocin and CD2AP,participating in signal transduction and maintaining podocytes normal construction and function.Mutations in TRPC6 cause autosomal dominant familial focal segmental glomerulosclerosis which is characterized by grade proteinuria and podocyte injury.In vitro studies,it also indicates that overexpression of TRPC6 leads to podocyte dysfunction,maybe through elevating calcium influx,suggesting that TRPC6 associates with the onset and development of proteinuria.This article will describe the role of TRPC6 in podocyte injury,maybe provide us the new targets for diagnosing and theraping renal disorders in the future.
TRPC6
Nephrin
Podocin
Slit diaphragm
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The glomerular filtration barrier is a highly specialized tri-layer structure with unique functional properties. Podocyte dysfunction and cytoskeletal disorganization leads to disruption of the slit diaphragma, and proteinuria. Inflammatory diseases involving the kidney as well as inherited podocytopathies or diabetic nephropathy cause injury of the podocyte network. Focal segmental glomerulosclerosis (FSGS) is a pathologic entity that is a common cause of nephrotic syndrome with severe proteinuria in both adults and children. Several causative genes have been identified in the pathogenesis of FSGS. Mutations of the transient receptor potential canonical-6 (TRPC6), a non-selective cation channel that is directly activated by diacylglycerol (DAG), cause a particularly aggressive form of FSGS. Angiotensin II, acting through its AT1 receptor, plays a critical role in generation of proteinuria and progression of kidney injury in a number of kidney diseases, including FSGS. Mounting evidence suggest the central role of TRPC6 and perhaps other TRPC channels in the pathogenesis of FSGS as well as of acquired forms of proteinuria such as diabetic nephropathy or hypertension. Identification of signaling pathways downstream of TRPC6 may provide novel targets for the treatment of proteinuria and prevent progression of podocyte injury.
TRPC6
Glomerulosclerosis
Membranous Nephropathy
Albuminuria
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Transient receptor potential cation channel 6(TRPC6) is a nonselective cation channel,located in the podocyte cell membrane and contains six membrane-spanning domains.TRPC6 is associated with slit diaphragm proteins-nephrin and podocin,the three proteins composing the slit diaphragm complex.Mutant TRPC6 may affect the function of this complex,leading to abnormalities in podocyte foot processes.Research suggested that mutant TRPC6 closely correlated with the mechanism of hereditary and non-hereditary nephropathies,possibly by altering podocyte dynamics and decreasing podocyte number.Blocking TRPC6 channels might be of therapeutic effect in treating kidney disease with proteinuria,and it may translate into long-lasting clinical benefits in patients with nephropathy.
TRPC6
Nephrin
Slit diaphragm
Podocin
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<b><i>Background:</i></b> Focal segmental glomerulosclerosis (FSGS) is a histologic pattern characterized by focal glomerular scarring, which often progresses to systemic and diffuse glomerulosclerosis. Previous studies have emphasized that the initiation of classic FSGS occurs in podocytes. The dysfunction and loss of podocytes have been associated with the development of proteinuria and the progression of various diseases. In addition, primary, secondary, and genetic FSGS are caused by different mechanisms of podocyte injury. <b><i>Summary:</i></b> The potential sources and mechanism of podocyte supplementation are the focus of our current research. Increasing attention has been paid to the role played by parietal epithelial cells (PECs) during the progression of FSGS. PECs are not only the primary influencing factors in glomerulosclerosis lesions but also have repair abilities, which remain a focus of debate. Notably, other resident glomerular cells also play significant roles in the progression of this disease. <b><i>Key Message:</i></b> In this review, we focus on the mechanism of scarring in FSGS and discuss current and potential therapeutic strategies.
Glomerulosclerosis
Minimal change disease
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Objective: In this study, we investigated the molecule mechanisms of podocyte injury and proteinuria and the protective effects of losartan. Methods: This study set up three groups: a control group; an Ang II group (Ang II 10 –6 mol/l, Sigma); and a losartan group (losartan 10 –6 mol/l, Sigma). We used RT-PCR assay to detect TRPC6 mRNA expression, and Western blot to detect TRPC6 protein expression. Results: TRPC6 overexpression was the basic change of podocyte injury and proteinuria occurrence. Losartan can treat podocyte injury and proteinuria induced by Ang II via downregulation of TRPC6 in podocytes. Conclusion: These findings maybe provide an ideal drug target for the diagnosis and treatment of acquired glomerular diseases.
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Glomerulosclerosis
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