-
1
-
-
84855183026
-
Focal segmental glomerulosclerosis
-
D́Agati VD, Kaskel FJ, Falk RJ. Focal segmental glomerulosclerosis. N Engl J Med. 2011; 365(25):2398-2411
-
(2011)
N Engl J Med
, vol.365
, Issue.25
, pp. 2398-2411
-
-
D́agati, V.D.1
Kaskel, F.J.2
Falk, R.J.3
-
2
-
-
22844436647
-
TRPC6 is a glomerular slit diaphragm- associated channel required for normal renal function
-
Reiser J, et al. TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet. 2005;37(7):739-744
-
(2005)
Nat Genet
, vol.37
, Issue.7
, pp. 739-744
-
-
Reiser, J.1
-
3
-
-
20844461826
-
A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis
-
Winn MP, et al. A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. Science. 2005;308(5729):1801-1804
-
(2005)
Science
, vol.308
, Issue.5729
, pp. 1801-1804
-
-
Winn, M.P.1
-
4
-
-
0032015551
-
Positionally cloned gene for a novel glomerular protein - nephrin - is mutated in congenital nephrotic syndrome
-
Kestilä M, et al. Positionally cloned gene for a novel glomerular protein - nephrin - is mutated in congenital nephrotic syndrome. Mol Cell. 1998; 1(4):575-582
-
(1998)
Mol Cell
, vol.1
, Issue.4
, pp. 575-582
-
-
Kestilä, M.1
-
5
-
-
73349132341
-
Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis
-
Brown EJ, et al. Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis. Nat Genet. 2010;42(1):72-76
-
(2010)
Nat Genet
, vol.42
, Issue.1
, pp. 72-76
-
-
Brown, E.J.1
-
6
-
-
84865788310
-
Signaling from the podocyte intercellular junction to the actin cytoskeleton
-
George B, Holzman LB. Signaling from the podocyte intercellular junction to the actin cytoskeleton. Semin Nephrol. 2012;32(4):307-318
-
(2012)
Semin Nephrol
, vol.32
, Issue.4
, pp. 307-318
-
-
George, B.1
Holzman, L.B.2
-
7
-
-
34250006557
-
The spectrum of podocytopathies: A unifying view of glomerular diseases
-
Wiggins RC. The spectrum of podocytopathies: a unifying view of glomerular diseases. Kidney Int. 2007;71(12):1205-1214
-
(2007)
Kidney Int
, vol.71
, Issue.12
, pp. 1205-1214
-
-
Wiggins, R.C.1
-
8
-
-
33644783770
-
Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy
-
Susztak K, Raff AC, Schiffer M, Böttinger EP. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes. 2006;55(1):225-233
-
(2006)
Diabetes
, vol.55
, Issue.1
, pp. 225-233
-
-
Susztak, K.1
Raff, A.C.2
Schiffer, M.3
Böttinger, E.P.4
-
9
-
-
40449112321
-
The Notch pathway in podocytes plays a role in the development of glomerular disease
-
Niranjan T, et al. The Notch pathway in podocytes plays a role in the development of glomerular disease. Nat Med. 2008;14(3):290-298
-
(2008)
Nat Med
, vol.14
, Issue.3
, pp. 290-298
-
-
Niranjan, T.1
-
10
-
-
79957881425
-
Role of mTOR in podocyte function and diabetic nephropathy in humans and mice
-
Gödel M, et al. Role of mTOR in podocyte function and diabetic nephropathy in humans and mice. J Clin Invest. 2011;121(6):2197-2209
-
(2011)
J Clin Invest
, vol.121
, Issue.6
, pp. 2197-2209
-
-
Gödel, M.1
-
11
-
-
59249092391
-
A systematic approach to mapping recessive disease genes in individuals from outbred populations
-
Hildebrandt F, et al. A systematic approach to mapping recessive disease genes in individuals from outbred populations. PLoS Genet. 2009; 5(1):e1000353
-
(2009)
PLoS Genet
, vol.5
, Issue.1
-
-
Hildebrandt, F.1
-
12
-
-
84890038202
-
10 biosynthesis disruption
-
10 biosynthesis disruption. J Clin Invest. 2013; 123(12):5179-5189
-
(2013)
J Clin Invest
, vol.123
, Issue.12
, pp. 5179-5189
-
-
Ashraf, S.1
-
13
-
-
34250668197
-
COQ2 nephropathy: A newly described inherited mitochondriopathy with primary renal involvement
-
Diomedi-Camassei F, et al. COQ2 nephropathy: a newly described inherited mitochondriopathy with primary renal involvement. J Am Soc Nephrol. 2007; 18(10):2773-2780
-
(2007)
J Am Soc Nephrol
, vol.18
, Issue.10
, pp. 2773-2780
-
-
Diomedi-Camassei, F.1
-
14
-
-
79955520308
-
COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness
-
Heeringa SF, et al. COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness. J Clin Invest. 2011;121(5):2013-2024
-
(2011)
J Clin Invest
, vol.121
, Issue.5
, pp. 2013-2024
-
-
Heeringa, S.F.1
-
15
-
-
33845232634
-
Leigh syndrome with nephropathy and CoQ10 deficiency due to decaprenyl diphosphate synthase subunit 2 (PDSS2) mutations
-
López LC, et al. Leigh syndrome with nephropathy and CoQ10 deficiency due to decaprenyl diphosphate synthase subunit 2 (PDSS2) mutations. Am J Hum Genet. 2006;79(6):1125-1129
-
(2006)
Am J Hum Genet
, vol.79
, Issue.6
, pp. 1125-1129
-
-
López, L.C.1
-
16
-
-
57349192861
-
Coenzyme Q10 supplementation rescues renal disease in Pdss2kd/kd mice with mutations in prenyl diphosphate synthase subunit 2
-
Saiki R, et al. Coenzyme Q10 supplementation rescues renal disease in Pdss2kd/kd mice with mutations in prenyl diphosphate synthase subunit 2. Am J Physiol Renal Physiol. 2008; 295(5):F1535-F1544
-
(2008)
Am J Physiol Renal Physiol
, vol.295
, Issue.5
-
-
Saiki, R.1
-
17
-
-
84856239775
-
Ubiquinone (coenzyme Q10) prevents renal mitochondrial dysfunction in an experimental model of type 2 diabetes
-
Sourris KC, et al. Ubiquinone (coenzyme Q10) prevents renal mitochondrial dysfunction in an experimental model of type 2 diabetes. Free Radic Biol Med. 2012;52(3):716-723
-
(2012)
Free Radic Biol Med
, vol.52
, Issue.3
, pp. 716-723
-
-
Sourris, K.C.1
-
18
-
-
84862528769
-
Coenzyme Q10 prevents GDPsensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes
-
Persson MF, et al. Coenzyme Q10 prevents GDPsensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes. Diabetologia. 2012;55(5):1535-1543
-
(2012)
Diabetologia
, vol.55
, Issue.5
, pp. 1535-1543
-
-
Persson, M.F.1
|