Role of TRPC6 in Progression of Diabetic Kidney Disease.

作者: Alexander Staruschenko , Denisha Spires , Oleg Palygin

DOI: 10.1007/S11906-019-0960-9

关键词:

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.

参考文章(105)
J Štekrová, J Reiterová, H Šafránková, M Kohoutová, L Obeidová, V Tesař, P Lněnička, TRPC6 gene variants in Czech adult patients with focal segmental glomerulosclerosis and minimal change disease. Folia Biologica. ,vol. 58, pp. 173- 176 ,(2012)
Marc Anderson, Hila Roshanravan, Justin Khine, Stuart E. Dryer, Angiotensin II activation of TRPC6 channels in rat podocytes requires generation of reactive oxygen species. Journal of Cellular Physiology. ,vol. 229, pp. 434- 442 ,(2014) , 10.1002/JCP.24461
Alexander Dietrich, Thomas Gudermann, TRPC6: Physiological Function and Pathophysiological Relevance Handbook of Experimental Pharmacology. ,vol. 222, pp. 157- 188 ,(2014) , 10.1007/978-3-642-54215-2_7
Anja K. Büscher, Martin Konrad, Mato Nagel, Oliver Witzke, Andreas Kribben, Peter F. Hoyer, Stefanie Weber, Mutations in podocyte genes are a rare cause of primary FSGS associated with ESRD in adult patients. Clinical Nephrology. ,vol. 78, pp. 47- 53 ,(2012) , 10.5414/CN107320
Julia M. Hofstra, Marieke J. H. Coenen, Mascha M. V. A. P. Schijvenaars, Jo H. M. Berden, Johan van der Vlag, Lies H. Hoefsloot, Nine V. A. M. Knoers, Jack F. M. Wetzels, Tom Nijenhuis, TRPC6 Single Nucleotide Polymorphisms and Progression of Idiopathic Membranous Nephropathy PLoS ONE. ,vol. 9, pp. e102065- ,(2014) , 10.1371/JOURNAL.PONE.0102065
Y. Liao, N. W. Plummer, M. D. George, J. Abramowitz, M. X. Zhu, L. Birnbaumer, A role for Orai in TRPC-mediated Ca2+ entry suggests that a TRPC:Orai complex may mediate store and receptor operated Ca2+ entry Proceedings of the National Academy of Sciences of the United States of America. ,vol. 106, pp. 3202- 3206 ,(2009) , 10.1073/PNAS.0813346106
Stephanie Toth-Manikowski, Mohamed G. Atta, Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets Experimental Diabetes Research. ,vol. 2015, pp. 697010- 697010 ,(2015) , 10.1155/2015/697010
K A Bauer, L M Weiss, D Sparrow, P S Vokonas, R D Rosenberg, Aging-associated changes in indices of thrombin generation and protein C activation in humans. Normative Aging Study. Journal of Clinical Investigation. ,vol. 80, pp. 1527- 1534 ,(1987) , 10.1172/JCI113238
Y. Kitamoto, K. Tomita, T. Imamura, Assessment of thrombin in the urine of glomerulonephritic patients by enzyme-linked immunosorbent assay Annals of Clinical Biochemistry. ,vol. 41, pp. 133- 137 ,(2004) , 10.1258/000456304322880023
Vincent G. DeMarco, Annayya R. Aroor, James R. Sowers, The pathophysiology of hypertension in patients with obesity Nature Reviews Endocrinology. ,vol. 10, pp. 364- 376 ,(2014) , 10.1038/NRENDO.2014.44